PI3K inhib News - LARVOL Sigma

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|||||||||| pictilisib (GDC-0941) / Roche, buparlisib (BKM120) / Novartis, Adlai Nortye
[VIRTUAL] Impact of PI3K inhibition in AIs-treated sensitive and resistant breast cancer cells: anti-proliferative effects and induction of apoptosis () - May 30, 2021 - Abstract #EACR2021EACR_1688;
The third-generation of aromatase inhibitors (AIs), anastrozole (Ana), letrozole (Let) and exemestane (Exe) are a first-line treatment option for estrogen receptor-positive (ER+ ) breast tumors, in postmenopausal women...Therefore, in this work the combinations of two PI3K class I inhibitors, buparlisib (BKM120) and pictilisib (GDC-0941), with AIs were explored in AIs-sensitive (MCF-7aro) and AIs-resistant (LTEDaro) breast cancer cell models...All the combinations in the resistant cells induced apoptosis, through mitochondrial pathway, with a more pronounced effect for the combinations with Exe. Conclusion Despite the high toxicity associated with the use of PI3K class I inhibitors, these results support further studies combining new, less toxic and specific PI3K class I inhibitors with AIs, especially with Exe, in refractory ER+ tumors The authors thank Fundação para a Ciência e Tecnologia (FCT) for T. Augusto PhD grant (BD/128333/2017) funded in part by FCT PhD Programme in Medicines and Pharmaceutical Innovation (i3DU), for C. Amaral contract (DL 57/2016 – Norma Transitória) and by Post-doc grant (SFRH/BPD/98304/2013) and for financial support (UIDP/04378/2020, UIDB/04378/2020).

|||||||||| [VIRTUAL] PI3K-C2G Loss Promotes Pancreatic Cancer via Glutamine-dependent mTOR Regulation () - May 30, 2021 - Abstract #EACR2021EACR_1263;
This was replicated through the administration of glutaminase inhibitors, demonstrating a translatable means to unveil new therapeutic strategies for PC treatment. Conclusion These findings establish PI3K-C2G as a tumor suppressor and suggest that the metabolic phenotype of PI3K-C2G-deficient tumors can be exploited by specific therapeutic strategies.

|||||||||| [VIRTUAL] PI3K-C2G Loss Promotes Pancreatic Cancer via Glutamine-dependent mTOR Regulation () - May 30, 2021 - Abstract #EACR2021EACR_1262;
This was replicated through the administration of glutaminase inhibitors, demonstrating a translatable means to unveil new therapeutic strategies for PC treatment. Conclusion These findings establish PI3K-C2G as a tumor suppressor and suggest that the metabolic phenotype of PI3K-C2G-deficient tumors can be exploited by specific therapeutic strategies.

|||||||||| [VIRTUAL] PI3K-C2G Loss Promotes Pancreatic Cancer via Glutamine-dependent mTOR Regulation () - May 30, 2021 - Abstract #EACR2021EACR_1261;
This was replicated through the administration of glutaminase inhibitors, demonstrating a translatable means to unveil new therapeutic strategies for PC treatment. Conclusion These findings establish PI3K-C2G as a tumor suppressor and suggest that the metabolic phenotype of PI3K-C2G-deficient tumors can be exploited by specific therapeutic strategies.

|||||||||| [VIRTUAL] PI3K-C2G Loss Promotes Pancreatic Cancer via Glutamine-dependent mTOR Regulation () - May 30, 2021 - Abstract #EACR2021EACR_1260;
This was replicated through the administration of glutaminase inhibitors, demonstrating a translatable means to unveil new therapeutic strategies for PC treatment. Conclusion These findings establish PI3K-C2G as a tumor suppressor and suggest that the metabolic phenotype of PI3K-C2G-deficient tumors can be exploited by specific therapeutic strategies.

|||||||||| [VIRTUAL] Role of PI3K-C2α/Rab11 axis in breast cancer progression () - May 30, 2021 - Abstract #EACR2021EACR_1123;
These results highlight the importance of PI3K-C2α/Rab11 axis in cancer cell progression. Conclusion In conclusion, we demonstrate that enhanced PI3K-C2α-dependent PI3P production in a panel of human BC cells increases Rab11 activity resulting in enhanced migratory and invasive capacity.

|||||||||| [VIRTUAL] Role of PI3K-C2α/Rab11 axis in breast cancer progression () - May 30, 2021 - Abstract #EACR2021EACR_1122;
These results highlight the importance of PI3K-C2α/Rab11 axis in cancer cell progression. Conclusion In conclusion, we demonstrate that enhanced PI3K-C2α-dependent PI3P production in a panel of human BC cells increases Rab11 activity resulting in enhanced migratory and invasive capacity.

|||||||||| [VIRTUAL] Role of PI3K-C2α/Rab11 axis in breast cancer progression () - May 30, 2021 - Abstract #EACR2021EACR_1121;
These results highlight the importance of PI3K-C2α/Rab11 axis in cancer cell progression. Conclusion In conclusion, we demonstrate that enhanced PI3K-C2α-dependent PI3P production in a panel of human BC cells increases Rab11 activity resulting in enhanced migratory and invasive capacity.

|||||||||| [VIRTUAL] Role of PI3K-C2α/Rab11 axis in breast cancer progression () - May 30, 2021 - Abstract #EACR2021EACR_1120;
These results highlight the importance of PI3K-C2α/Rab11 axis in cancer cell progression. Conclusion In conclusion, we demonstrate that enhanced PI3K-C2α-dependent PI3P production in a panel of human BC cells increases Rab11 activity resulting in enhanced migratory and invasive capacity.

|||||||||| [VIRTUAL] PI3K-C2α promotes breast cancer metastasis by regulating focal adhesion dynamics () - May 30, 2021 - Abstract #EACR2021EACR_1111;
Rescue experiments performed with a kinase-inactive (KD) or only PI(3)P producing form of PI3K-C2α revealed that the increased migration and invasion ability specifically relies on the production of PI(3,4)P2 at FA Conclusion We showed that PI3K-C2α promoted EMT and increased BC cell migration and invasion by controlling FAK activation. In line with these findings, we demonstrated that increased PI3K-C2α expression accelerated FA disassembly at plasma membrane in a PI(3,4)P2 dependent manner, highlighting a potential role for PI3K-C2α as a predictive biomarker for BC metastasis prognosis.

|||||||||| [VIRTUAL] PI3K-C2α promotes breast cancer metastasis by regulating focal adhesion dynamics () - May 30, 2021 - Abstract #EACR2021EACR_1110;
Rescue experiments performed with a kinase-inactive (KD) or only PI(3)P producing form of PI3K-C2α revealed that the increased migration and invasion ability specifically relies on the production of PI(3,4)P2 at FA Conclusion We showed that PI3K-C2α promoted EMT and increased BC cell migration and invasion by controlling FAK activation. In line with these findings, we demonstrated that increased PI3K-C2α expression accelerated FA disassembly at plasma membrane in a PI(3,4)P2 dependent manner, highlighting a potential role for PI3K-C2α as a predictive biomarker for BC metastasis prognosis.

|||||||||| [VIRTUAL] PI3K-C2α promotes breast cancer metastasis by regulating focal adhesion dynamics () - May 30, 2021 - Abstract #EACR2021EACR_1109;
Rescue experiments performed with a kinase-inactive (KD) or only PI(3)P producing form of PI3K-C2α revealed that the increased migration and invasion ability specifically relies on the production of PI(3,4)P2 at FA Conclusion We showed that PI3K-C2α promoted EMT and increased BC cell migration and invasion by controlling FAK activation. In line with these findings, we demonstrated that increased PI3K-C2α expression accelerated FA disassembly at plasma membrane in a PI(3,4)P2 dependent manner, highlighting a potential role for PI3K-C2α as a predictive biomarker for BC metastasis prognosis.

|||||||||| [VIRTUAL] PI3K-C2α promotes breast cancer metastasis by regulating focal adhesion dynamics () - May 30, 2021 - Abstract #EACR2021EACR_1108;
Rescue experiments performed with a kinase-inactive (KD) or only PI(3)P producing form of PI3K-C2α revealed that the increased migration and invasion ability specifically relies on the production of PI(3,4)P2 at FA Conclusion We showed that PI3K-C2α promoted EMT and increased BC cell migration and invasion by controlling FAK activation. In line with these findings, we demonstrated that increased PI3K-C2α expression accelerated FA disassembly at plasma membrane in a PI(3,4)P2 dependent manner, highlighting a potential role for PI3K-C2α as a predictive biomarker for BC metastasis prognosis.

|||||||||| cisplatin / Generic mfg.
[VIRTUAL] Gallic acid induced the cell cycle arrest and apoptosis in A549 lung cancer cells via PI3K/Akt pathway () - May 30, 2021 - Abstract #EACR2021EACR_851;
This study elucidates the anti-cancer potential of gallic acid (GA) as a promising therapeutic agent that exerts its effect by regulating the PI3K/Akt pathway, and focusing on the inhibition of survival and induction of apoptosis in A549 cells, as compared to cisplatin (CDDP)...Intraperitoneal (IP) injection with GA and CDDP for 4 weeks in an A549-derived tumor xenograft model reduced the size of tumor mass and downregulated the expression of proliferating cell nuclear antigen (PCNA) and p-Akt, but upregulated the expression of Cleaved caspase-3 in tumor tissues. Conclusion Taken together, these results indicated that GA hindered lung cancer progression by inducing cell cycle arrest and apoptosis, suggesting that GA would be a potential promising therapeutic agent against NSCLC.

|||||||||| cisplatin / Generic mfg.
[VIRTUAL] Gallic acid induced the cell cycle arrest and apoptosis in A549 lung cancer cells via PI3K/Akt pathway () - May 30, 2021 - Abstract #EACR2021EACR_850;
This study elucidates the anti-cancer potential of gallic acid (GA) as a promising therapeutic agent that exerts its effect by regulating the PI3K/Akt pathway, and focusing on the inhibition of survival and induction of apoptosis in A549 cells, as compared to cisplatin (CDDP)...Intraperitoneal (IP) injection with GA and CDDP for 4 weeks in an A549-derived tumor xenograft model reduced the size of tumor mass and downregulated the expression of proliferating cell nuclear antigen (PCNA) and p-Akt, but upregulated the expression of Cleaved caspase-3 in tumor tissues. Conclusion Taken together, these results indicated that GA hindered lung cancer progression by inducing cell cycle arrest and apoptosis, suggesting that GA would be a potential promising therapeutic agent against NSCLC.

|||||||||| cisplatin / Generic mfg.
[VIRTUAL] Gallic acid induced the cell cycle arrest and apoptosis in A549 lung cancer cells via PI3K/Akt pathway () - May 30, 2021 - Abstract #EACR2021EACR_849;
This study elucidates the anti-cancer potential of gallic acid (GA) as a promising therapeutic agent that exerts its effect by regulating the PI3K/Akt pathway, and focusing on the inhibition of survival and induction of apoptosis in A549 cells, as compared to cisplatin (CDDP)...Intraperitoneal (IP) injection with GA and CDDP for 4 weeks in an A549-derived tumor xenograft model reduced the size of tumor mass and downregulated the expression of proliferating cell nuclear antigen (PCNA) and p-Akt, but upregulated the expression of Cleaved caspase-3 in tumor tissues. Conclusion Taken together, these results indicated that GA hindered lung cancer progression by inducing cell cycle arrest and apoptosis, suggesting that GA would be a potential promising therapeutic agent against NSCLC.

|||||||||| cisplatin / Generic mfg.
[VIRTUAL] Gallic acid induced the cell cycle arrest and apoptosis in A549 lung cancer cells via PI3K/Akt pathway () - May 30, 2021 - Abstract #EACR2021EACR_848;
This study elucidates the anti-cancer potential of gallic acid (GA) as a promising therapeutic agent that exerts its effect by regulating the PI3K/Akt pathway, and focusing on the inhibition of survival and induction of apoptosis in A549 cells, as compared to cisplatin (CDDP)...Intraperitoneal (IP) injection with GA and CDDP for 4 weeks in an A549-derived tumor xenograft model reduced the size of tumor mass and downregulated the expression of proliferating cell nuclear antigen (PCNA) and p-Akt, but upregulated the expression of Cleaved caspase-3 in tumor tissues. Conclusion Taken together, these results indicated that GA hindered lung cancer progression by inducing cell cycle arrest and apoptosis, suggesting that GA would be a potential promising therapeutic agent against NSCLC.

|||||||||| [VIRTUAL] Using a multidisciplinary, “quantitative cell biology toolbox” to link changes in epithelial morphogenesis and oncogenic Ras/Erk and PI3K/Akt mutations () - May 30, 2021 - Abstract #EACR2021EACR_843;
Currently, we apply this approach to study multiple oncogenic mutations in Ras/Erk and PI3K/Akt pathways to understand how these mutations lead to distinct aberrant morphologies. Conclusion Using “quantitative cell biology toolbox” we expect to identify how different mutations in Ras/Erk and PI3K/Akt signalling pathways lead to aberrant spatio-temporal Erk and Akt signalling that induces abnormal mammary morphogenesis.

|||||||||| [VIRTUAL] Using a multidisciplinary, “quantitative cell biology toolbox” to link changes in epithelial morphogenesis and oncogenic Ras/Erk and PI3K/Akt mutations () - May 30, 2021 - Abstract #EACR2021EACR_842;
Currently, we apply this approach to study multiple oncogenic mutations in Ras/Erk and PI3K/Akt pathways to understand how these mutations lead to distinct aberrant morphologies. Conclusion Using “quantitative cell biology toolbox” we expect to identify how different mutations in Ras/Erk and PI3K/Akt signalling pathways lead to aberrant spatio-temporal Erk and Akt signalling that induces abnormal mammary morphogenesis.

|||||||||| [VIRTUAL] Using a multidisciplinary, “quantitative cell biology toolbox” to link changes in epithelial morphogenesis and oncogenic Ras/Erk and PI3K/Akt mutations () - May 30, 2021 - Abstract #EACR2021EACR_841;
Currently, we apply this approach to study multiple oncogenic mutations in Ras/Erk and PI3K/Akt pathways to understand how these mutations lead to distinct aberrant morphologies. Conclusion Using “quantitative cell biology toolbox” we expect to identify how different mutations in Ras/Erk and PI3K/Akt signalling pathways lead to aberrant spatio-temporal Erk and Akt signalling that induces abnormal mammary morphogenesis.

|||||||||| [VIRTUAL] Using a multidisciplinary, “quantitative cell biology toolbox” to link changes in epithelial morphogenesis and oncogenic Ras/Erk and PI3K/Akt mutations () - May 30, 2021 - Abstract #EACR2021EACR_840;
Currently, we apply this approach to study multiple oncogenic mutations in Ras/Erk and PI3K/Akt pathways to understand how these mutations lead to distinct aberrant morphologies. Conclusion Using “quantitative cell biology toolbox” we expect to identify how different mutations in Ras/Erk and PI3K/Akt signalling pathways lead to aberrant spatio-temporal Erk and Akt signalling that induces abnormal mammary morphogenesis.

|||||||||| [VIRTUAL] Role of PI3K and mTOR in triple-negative breast cancer () - May 30, 2021 - Abstract #EACR2021EACR_487;
We provide evidence that the PAM pathway activation might have a major role in TNBC progression and is connected with poor clinical course. Our results support the value of the PAM pathway as a target for future TNBC therapies.

|||||||||| [VIRTUAL] Role of PI3K and mTOR in triple-negative breast cancer () - May 30, 2021 - Abstract #EACR2021EACR_486;
We provide evidence that the PAM pathway activation might have a major role in TNBC progression and is connected with poor clinical course. Our results support the value of the PAM pathway as a target for future TNBC therapies.

|||||||||| [VIRTUAL] Role of PI3K and mTOR in triple-negative breast cancer () - May 30, 2021 - Abstract #EACR2021EACR_485;
We provide evidence that the PAM pathway activation might have a major role in TNBC progression and is connected with poor clinical course. Our results support the value of the PAM pathway as a target for future TNBC therapies.

|||||||||| [VIRTUAL] Role of PI3K and mTOR in triple-negative breast cancer () - May 30, 2021 - Abstract #EACR2021EACR_484;
We provide evidence that the PAM pathway activation might have a major role in TNBC progression and is connected with poor clinical course. Our results support the value of the PAM pathway as a target for future TNBC therapies.

|||||||||| Jakafi oral (ruxolitinib) / Novartis, Incyte, parsaclisib (INCB50465) / Incyte
.@AYACOUB7 , MD, of @KUMedCenter discusses the rationale for combining PI3K inhibitors with ruxolitinib in myelofibrosis, the results of the phase 2 study with parsaclisib, and ongoing phase 3 trials evaluating this novel combination. https://t.co/b4Em4OlyvM (Twitter) - May 30, 2021

|||||||||| quercetin (LY294002) / Eli Lilly
Journal: A novel marine halophenol derivative attenuates lipopolysaccharide-induced inflammation in RAW264.7 cells via activating phosphoinositide 3-kinase/Akt pathway. (Pubmed Central) - May 29, 2021
In this study, we demonstrated that a halophenol derivative (LM49) could possess anti-inflammatory activity on LPS-stimulated RAW264.7 cells by reducing pro-inflammatory cytokines and enhancing the phagocytic capacity, in which the PI3K/Akt pathway plays an essential role. LM49 may have clinical utility as an anti-inflammatory agent.

|||||||||| Aliqopa (copanlisib) / Bayer
Journal: Copanlisib: Novel PI3K Inhibitor for Treatment of Lymphoma. (Pubmed Central) - May 29, 2021
In the present review various aspects related to Copanlisib have been summarized which include pathophysiology, synthetic strategy, pharmacokinetics, pharmacodynamics and clinical studies. A special emphasis is given on various reported adverse effect and in silico/ in vivo studies conducted on Copanlisib.

|||||||||| Cabometyx (cabozantinib tablet) / Takeda, Exelixis, Ipsen
Clinical, Journal: Case report for an adolescent with germline RET mutation and alveolar rhabdomyosarcoma. (Pubmed Central) - May 29, 2021
We also evaluated the use of JAK/STAT pathway inhibitors in the context of rhabdomyosarcomas bearing the FGFR4 G388R coding variant. Although the patient succumbed to his disease, study of the patient's tumor has generated insights into the biology of RET and other targets in rhabdomyosarcoma.

|||||||||| Preclinical, Journal: Protective role of microRNA-27a upregulation and HSP90 silencing against cerebral ischemia-reperfusion injury in rats by activating PI3K/AKT/mTOR signaling pathway. (Pubmed Central) - May 29, 2021
Although the patient succumbed to his disease, study of the patient's tumor has generated insights into the biology of RET and other targets in rhabdomyosarcoma. To conclude, our study demonstrates that elevated miR-27a or decreased HSP90 attenuates oxidative stress and inflammatory response, and improves neurological function in cerebral ischemia-reperfusion injury rats by activating PI3K/AKT/mTOR signaling pathway.

|||||||||| Journal: ISLR regulates skeletal muscle atrophy via IGF1-PI3K/Akt-Foxo signaling pathway. (Pubmed Central) - May 29, 2021
Meanwhile, the expression of caspase-8 and caspase-9 increased in Islr-silenced groups, indicating its role in cell viability. Taken together, these data suggested that Islr plays an important role in myoblasts differentiation, and which can alleviate skeletal muscle atrophy and prevents muscle cell apoptosis via IGF/PI3K/AKT-FOXO signaling pathway.

|||||||||| cisplatin / Generic mfg.
Journal: PSAT1 Upregulation Contributes to Cell Growth and Cisplatin Resistance in Cervical Cancer Cells via Regulating PI3K/AKT Signaling Pathway. (Pubmed Central) - May 29, 2021
Inhibition of PSAT1 reduced cisplatin resistance in SiHa-R cells through suppressing proliferation and inducing apoptosis by blocking PI3K/Akt signaling pathway. PSAT1 may be a potential therapeutic target to reverse chemoresistance in cisplatin-resistant CC.

|||||||||| quercetin (LY294002) / Eli Lilly
Journal: IRS-2/Akt/GSK-3β/Nrf2 Pathway Contributes to the Protective Effects of Chikusetsu Saponin IVa against Lipotoxicity. (Pubmed Central) - May 29, 2021
Furthermore, siRNA-targeted Nrf2, PI3K/Akt inhibitor (LY294002), or GSK-3β inhibitor (LiCl) was used to investigate the crosstalk relationships between proteins...In addition, inhibition of PI3K/Akt or GSK-3β with specific inhibitors dramatically abrogated the protective effects of CHS, revealing that the IRS-2/Akt/GSK-3β signaling axis was involved in the protective effects of CHS. These results demonstrate that CHS protected βTC3 cells against PA-induced oxidative stress and cell dysfunction through Nrf2 by the IRS-2/Akt/GSK-3β-mediated pathway.

|||||||||| Journal, Epigenetic controller: Epidermal Growth Factor Protects Against High Glucose-Induced Podocyte Injury Possibly via Modulation of Autophagy and PI3K/AKT/mTOR Signaling Pathway Through DNA Methylation. (Pubmed Central) - May 29, 2021
In summary, our results demonstrated that EGF exerted protective effects on HG-induced podocytes injury via enhancing cell proliferation and inhibiting cell apoptosis. Further mechanistic studies implied that EGF-mediated protective effects in HG-stimulated podocytes may be associated with modulation of autophagy and PI3K/AKT/mTOR signaling pathway.

|||||||||| quercetin (LY294002) / Eli Lilly
Journal: Knockdown of NOLC1 Inhibits PI3K-AKT Pathway to Improve the Poor Prognosis of Esophageal Carcinoma. (Pubmed Central) - May 29, 2021
A recombined lentiviral vector containing NOLC1 was applied for transfecting ESCA cells (Eca109 and TE-13) and established a stable cell line with low NOLC1 expression or high NOLC1 expression, in the absence or presence of PI3K inhibitor (LY294002) treatment...NOLC1 may be a marker for poor prognosis. It can participate in the occurrence and development of ESCA via the PI3K/AKT pathway.

|||||||||| cisplatin / Generic mfg., docetaxel / Generic mfg.
Journal: Targeted Therapy With PI3K and FGFR Inhibitors on Human Papillomavirus Positive and Negative Tonsillar and Base of Tongue Cancer Lines With and Without Corresponding Mutations. (Pubmed Central) - May 29, 2021
Cisplatin and docetaxel also induced dose dependent responses, and upon combination with the inhibitors, both positive and neutral effects were found. The data suggest that FDA approved drugs alpelisib and erdafitinib efficiently inhibit TSCC/BOTSCC cell line growth, especially when combined irrespective of presence of corresponding mutations and should be further explored, for use upon recurrent disease.

|||||||||| cisplatin / Generic mfg.
Journal: Down-Regulating the Expression of miRNA-21 Inhibits the Glucose Metabolism of A549/DDP Cells and Promotes Cell Death Through the PI3K/AKT/mTOR/HIF-1α Pathway. (Pubmed Central) - May 29, 2021
Further investigations showed that miRNA-21 combined with cisplatin caused excessive inactivation of the pI3K/AKT/mTOR/HIF-1α signaling pathway in cisplatin-resistant A549/DDP cells. Hence, reduction of the expression of miRNA-21 in combination with cisplatin chemotherapy may effectively improve the therapeutic effect on patients with non-small cell lung cancer, and this may provide a theoretical basis for the treatment of this disease.

|||||||||| quercetin (LY294002) / Eli Lilly
[VIRTUAL] Aerobic Exercise Activated Irisin-PI3K-Akt Pathway To Inhibit Apoptosis In Skeletal Muscle Of Myocardial Infarction Mice () - May 29, 2021 - Abstract #ACSM2021ACSM_486;
Aerobic exercise inhibited apoptosis in skeletal muscle of myocardial infarction mice, partially via activating Irisin-PI3K-Akt signaling pathway. Supported by National Natural Science Foundation of China Grants (31671240).

|||||||||| Venclexta (venetoclax) / Roche, AbbVie, fimepinostat (CUDC-907) / Curis
Preclinical, Journal: The HDAC and PI3K dual inhibitor CUDC-907 synergistically enhances the antileukemic activity of venetoclax in preclinical models of acute myeloid leukemia. (Pubmed Central) - May 28, 2021
Interestingly, we found that venetoclax treatment enhances CUDC-907-induced DNA damage potentially through inhibition of DNA repair. In vivo results show that CUDC-907 enhances venetoclax efficacy in an acute myeloid leukemia cell line derived xenograft mouse model, supporting the development of CUDC-907 in combination with venetoclax for the treatment of acute myeloid leukemia.

|||||||||| Journal: Increased NDRG1 expression suppresses angiogenesis via PI3K/AKT pathway in human placental cells. (Pubmed Central) - May 28, 2021
In vivo results show that CUDC-907 enhances venetoclax efficacy in an acute myeloid leukemia cell line derived xenograft mouse model, supporting the development of CUDC-907 in combination with venetoclax for the treatment of acute myeloid leukemia. NDRG1 suppresses angiogenesis in preeclampsia, and the PI3K/AKT signaling pathway may be involved in the regulation of angiogenesis by NDRG1.

|||||||||| Journal, PARP Biomarker, IO biomarker: Inhibition of B7-H4 promotes hepatocellular carcinoma cell apoptosis and autophagy through the PI3K signaling pathway. (Pubmed Central) - May 28, 2021
Furthermore, our data revealed that B7-H4 regulated apoptosis and autophagy through the PI3K signaling pathway in HCC cells. Therefore, these results suggested that B7-H4 plays an important role in HCC progression by affecting cell apoptosis and autophagy.

|||||||||| Journal: Upregulation of Sirt1 by tyrosol suppresses apoptosis and inflammation and modulates extracellular matrix remodeling in interleukin-1β-stimulated human nucleus pulposus cells through activation of PI3K/Akt pathway. (Pubmed Central) - May 28, 2021
Sirt1 knockdown attenuated the effects of tyrosol on IL-1β-induced apoptosis, inflammation, and ECM remodeling in HNPCs. In summary, upregulation of Sirt1 by tyrosol suppressed apoptosis and inflammation and regulated ECM remodeling in IL-1β-stimulated HNPCs through activation of PI3K/Akt pathway.

|||||||||| Journal, PARP Biomarker, IO biomarker: Three phytosterols from sweet potato inhibit MCF7-xenograft-tumor growth through modulating gut microbiota homeostasis and SCFAs secretion. (Pubmed Central) - May 28, 2021
Our findings indicate that DLA, DL, and DP inhibit tumor growth in MCF-7 xenograft nude mice by regulating the homeostasis of gut microbiota, producing SCFAs, and then disturbing the expression of cancer-related proteins. The present study suggests three phytosterols as gut microbiota regulator for breast cancer prevention.

|||||||||| Preclinical, Journal: Chrysin Improves Glucose and Lipid Metabolism Disorders by Regulating the AMPK/PI3K/AKT Signaling Pathway in Insulin-Resistant HepG2 Cells and HFD/STZ-Induced C57BL/6J Mice. (Pubmed Central) - May 28, 2021
Treatment with the AMPK inhibitor verified that AMPK activation is positively correlated with chrysin activity on glycolipid metabolism. This study confirms that chrysin is a potential treatment for glucose and lipid metabolism disorders.

|||||||||| Ex-Rad (recilisib) / Onconova
Journal: Overexpression of microRNA-23a-5p induces myocardial infarction by promoting cardiomyocyte apoptosis through inhibited of PI3K/AKT signalling pathway. (Pubmed Central) - May 27, 2021
Recilisib-activated PI3K/Akt singling pathway could restrain apoptosis from inducing miR-23a-5p overexpression, and Miltefosine-blocked PI3K/Akt singling pathway could restrict apoptosis from inhibiting miR-23a-5p reduction. In conclusion, these findings revealed the pivotal role of miR-23a-5p-PI3K/Akt axis in regulating apoptosis during MI, introducing this novel axis as a potential indicator to detect ischemic heart disease and it could be used for therapeutic intervention.

|||||||||| Journal: PM impairs macrophage functions to exacerbate pneumococcus-induced pulmonary pathogenesis. (Pubmed Central) - May 27, 2021
In conclusion, these findings revealed the pivotal role of miR-23a-5p-PI3K/Akt axis in regulating apoptosis during MI, introducing this novel axis as a potential indicator to detect ischemic heart disease and it could be used for therapeutic intervention. The effect of PM exposure on macrophage activity enhances pneumococcal infectivity and aggravates pulmonary pathogenesis.

|||||||||| omipalisib (GSK2126458) / GSK
Journal: Omipalisib Inhibits Esophageal Squamous Cell Carcinoma Growth Through Inactivation of Phosphoinositide 3-Kinase (PI3K)/AKT/Mammalian Target of Rapamycin (mTOR) and ERK Signaling. (Pubmed Central) - May 27, 2021
The present study supports the rationale for using omipalisib as a therapeutic approach in ESCC patients. Further clinical studies are needed.

|||||||||| Journal: Pea-derived peptides, VLP, LLP, VA, and LL, improve insulin resistance in HepG2 cells via activating IRS-1/PI3K/AKT and blocking ROS-mediated p38MAPK signaling. (Pubmed Central) - May 27, 2021
PRACTICAL APPLICATIONS: This paper examined the intervention effect of VLP, LLP, VA, and LL that from pea on insulin resistance, and the mechanisms were detected by western blotting. The results provide a theoretical knowledge for the prevention of insulin resistance in T2D of pea-derived peptides and lay the foundation for the development of functional products and drugs in the future.

|||||||||| Journal: B and T lymphocyte attenuator regulates autophagy in mycobacterial infection via the AKT/mTOR signal pathway. (Pubmed Central) - May 27, 2021
Finally, treatment with BTLA agonist ameliorated lung pathology and promoted autophagy and mycobacterial clearance during mycobacterial infection in vivo. These results demonstrate that BTLA promotes host defense against mycobacteria by enhancing autophagy, which may provide potential therapeutic interventions against tuberculosis.

|||||||||| Venclexta (venetoclax) / Roche, AbbVie, quercetin (LY294002) / Eli Lilly
Journal, IO biomarker: Bcl-2 Is Involved in Cardiac Hypertrophy through PI3K-Akt Pathway. (Pubmed Central) - May 27, 2021
Furthermore, no matter LY294002, an inhibitor of the PI3K/AKT signaling pathway, or Venetoclax, a selective Bcl-2 inhibitor, protected against cardiac hypertrophy. In conclusion, these data indicate that Bcl-2 is involved in cardiac hypertrophy as a key downstream effector of PI3K-Akt signaling pathway, suggesting a potential therapeutic target for the clinical management of cardiac hypertrophy.



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