- |||||||||| MK-2206 / Merck (MSD), Mozobil (plerixafor) / Sanofi
Journal: SDF1/CXCR4 axis facilitates the angiogenesis via activating the PI3K/AKT pathway in degenerated discs. (Pubmed Central) - Apr 27, 2021 However, these effects induced by SDF1 overexpression in NPCs were all reversed when VECs were pretreated with AMD3100 or MK‑2206, whereas enhanced by SF1670 treatment. Collectively, the present study indicated that enhancement of the SDF1/CXCR4 axis in NPCs can significantly accelerate angiogenesis by regulating the PTEN/phosphatidylinositol‑3‑kinase/AKT pathway.
- |||||||||| docetaxel / Generic mfg.
Journal: Paired‑related homeobox 1 overexpression promotes multidrug resistance via PTEN/PI3K/AKT signaling in MCF‑7 breast cancer cells. (Pubmed Central) - Apr 27, 2021 The half‑maximal inhibitory concentration of three groups after treatment with docetaxel and cis‑platinum complexes were significantly higher in PRRX1‑overexpressing MCF‑7 cells compared with those in control cells...These results indicated that PRRX1 overexpression may induce MDR via PTEN/PI3K/AKT signaling in breast cancer. It is highly recommended that PRRX1 gene expression detection should be performed in patients with breast cancer to aid the selection of more appropriate treatments, which will lead to an improved prognosis in clinical practice.
- |||||||||| fluoxetine / Generic mfg.
Preclinical, Journal: Fluoxetine regulates glucose and lipid metabolism via the PI3K‑AKT signaling pathway in diabetic rats. (Pubmed Central) - Apr 27, 2021 Additionally, fluoxetine could inhibit the phosphatidylinositol 3‑kinase‑protein kinase B (PI3K‑AKT) signaling pathway, whereas LY294002, a specific inhibitor of PI3K, suppressed the function of PI3K‑AKT signaling and suppressed the expression levels of glucose metabolism‑associated proteins, including GSK‑3β, G6PC, PEPCK and FOXO1 in BRL‑3A cells. The results of the present study revealed that fluoxetine may regulate glucose and lipid metabolism via the PI3K‑AKT signaling pathway in diabetic rats.
- |||||||||| Journal: Ceramide-1-phosphate promotes the migration of retina Müller glial cells. (Pubmed Central) - Apr 27, 2021
These results suggest that C1P addition stimulated migration of glial Müller cells, promoting the activation of cPLA2, and the PI3K and ERK/MAPK pathways. They also suggest that CerK-dependent C1P synthesis was one of the factors contributing to glial migration, thus uncovering a novel role for C1P in controlling glial motility.
- |||||||||| PF-04691502 / Pfizer
Journal: Long non-coding RNA (lncRNA) H19 induces hepatic steatosis through activating MLXIPL and mTORC1 networks in hepatocytes. (Pubmed Central) - Apr 24, 2021 Furthermore, H19-induced lipid accumulation was effectively inhibited by PI3K/mTOR inhibitor PF-04691502...In vivo hepatocyte implantation studies further confirm that H19 promoted hepatic steatosis by up-regulating both mTORC1 signalling axis and MLXIPL transcriptional network. Collectively, these findings strongly suggest that H19 may play an important role in regulating hepatic lipid metabolism and may serve as a potential therapeutic target for NAFLD.
- |||||||||| Review, Journal: PI3K/AKT pathway as a key link modulates the multidrug resistance of cancers. (Pubmed Central) - Apr 24, 2021
This review highlights the aberrant activation of PI3K/AKT as a key link that modulates MDR. We summarize the regulation of numerous major targets correlated with the PI3K/AKT pathway, which is further related to MDR, including the expression of apoptosis-related protein, ABC transport and glycogen synthase kinase-3 beta (GSK-3β), synergism with nuclear factor kappa beta (NF-κB) and mammalian target of rapamycin (mTOR), and the regulation of glycolysis.
- |||||||||| cisplatin / Generic mfg., sirolimus / Generic mfg.
Journal, Cancer stem cells: mTOR Inhibition Ablates Cisplatin-Resistant Salivary Gland Cancer Stem Cells. (Pubmed Central) - Apr 24, 2021 Viability assays determined the effect of several inhibitors of PI3k/mTOR signaling (e.g., temsirolimus, BKM120, AZD8055, PF4708671) and/or cisplatin on survival of human MEC cells...Remarkably, temsirolimus slowed down tumor growth and decreased the fraction of CSCs (P < 0.05) even in presence of cisplatin in a short-term in vivo experiment. Collectively, these results demonstrate that therapeutic inhibition of mTOR ablates cytotoxic-resistant CSCs, and they suggest that a combination of an mTOR inhibitor and platinum-based chemotherapy might be beneficial to patients with salivary gland mucoepidermoid carcinoma.
- |||||||||| Aliqopa (copanlisib) / Bayer
Review, Journal: Update on the role of copanlisib in hematologic malignancies. (Pubmed Central) - Apr 24, 2021 The use of copanlisib as part of a combination therapy for various hematologic malignancies will also be discussed. Copanlisib is a unique drug compared with other PI3K inhibitors, with remarkable potential to improve our armamentarium in cancer treatment.
- |||||||||| gefitinib / Generic mfg.
Journal, IO biomarker: Linc01014 regulates gefitinib resistance in oesophagus cancer via EGFR-PI3K-AKT-mTOR signalling pathway. (Pubmed Central) - Apr 23, 2021 Overexpression of linc01014 significantly inhibited the apoptosis of FLO-1 cells induced by gefitinib and silencing linc01014 obviously promoted the apoptosis of FLO-1 cells induced by gefitinib. Silencing linc01014 could significantly increase the gefitinib chemotherapy sensitivity of oesophagus cancer via PI3K-AKT-mTOR signalling pathway.
- |||||||||| Erbitux (cetuximab) / Eli Lilly, EMD Serono, Aliqopa (copanlisib) / Bayer
Trial termination, Combination therapy, Metastases: COPAN-ORL06: Copanlisib in Association With Cetuximab in Patients With Recurrent and/or Metastatic Head and Neck Squamous Cell Carcinomas Harboring a PI3KCA Mutation/Amplification and/or a PTEN Loss (clinicaltrials.gov) - Apr 22, 2021 P1/2, N=11, Terminated, Our data demonstrated that ACTL8 may facilitate the proliferation, migration and invasion, while inhibiting apoptosis through activating PI3K/Akt/mTOR signaling pathway in TNBC. Active, not recruiting --> Terminated; futilty of the treatment
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