RETRACTED ARTICLE: Roles of the PI3K/AKT/mTOR signalling pathways in neurodegenerative diseases and tumours

Xu, Fei; Na, Lixin; Li, Yanfei; Chen, Linjun

doi:10.1186/s13578-020-00416-0

Cited by 469 publications

(290 citation statements)

References 116 publications

(127 reference statements)

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“…mTOR consists of two independent functional complexes, mTORC1 and mTORC2, which can be phosphorylated to p-mTOR regulating several cellular functions, including proliferation, differentiation, tumorigenesis, angiogenesis, autophagy, and apoptosis by activating ribosome biogenesis and protein synthesis. (20,21) In our study, we found reduced CENPO expression would downregulated the expression of PIK3CA and p-mTOR, suggesting CENPO may active PI3K/AKT/mTOR signaling pathway to promote cancer progression by avoiding apoptosis and other cellarbehaviors.…”

Section: Discussionmentioning

confidence: 49%

The role of CENPO expression in the progression of non-small cell lung cancer

Yang

Chen

Sun

et al. 2020

Preprint

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Background: The role of Centromere protein O (CENPO) in the development of non-small cell lung cancer (NSCLC) is unknown. This study aimed to investigate the potential roleof CENPO in the development of NSCLCMethods: The expression level of CENPO was investigated in both tissues and cell-lines. Celigo cell counting assay, wound-healing assay, Transwell assay and Flow cytometry was used to explore the effect of CENPO on proliferation, migration, invasion, apoptosis and cell cycle of NSCLC. The potential mechanism of CENPO was explored by Human Apoptosis Antibody, also, western blot was conducted to detect the expression of PI3K/Akt/mTOR pathway and cell-cycle related protein (mTOR, P-mTOR, CDK1, CDK6 and PIK3CA). Besides, the effect of CENPO on the growth of NSCLC solid tumors was demonstrated in vivo.Results: Our study suggested CENPO gene overexpression in NSCLC. Reduced CENPO expression substantially decreased the proliferation, migration and invasion ability, and promoting apoptosis and induces cell cycle arrest of NSCLC cell-lines. Preliminary mechanism research suggested reduced CENPO could active apoptosis pathway, suppressing PI3K/AKT/mTOR pathway and down-regulation cell-cycle related proteins.Conclusion: CENPO was up-regulated in NSCLC and played an important role in promoting the progress of NSCLC.

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Section: Discussionmentioning

confidence: 49%

The role of CENPO expression in the progression of non-small cell lung cancer

Yang

Chen

Sun

et al. 2020

Preprint

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“…In ovarian CSCs, ErbB4 receptor tyrosine kinase and STAT5 cooperate to promote the transcription of p85a and p110a, which are subunits of PI3K [ 16 ]. AKT is phosphorylated downstream of PI3K signaling [ 32 , 33 ], and ERK phosphorylation is enhanced by overexpression of the ErbB4 receptor [ 16 , 34 ]. The overexpressed L/T-type calcium channels increase calcium flow into the cytoplasm, which drives phosphorylation of AKT and ERK through PI3K and MAPK signaling [ 15 , 35 ].…”

Section: Discussionmentioning

confidence: 99%

Combined Poziotinib with Manidipine Treatment Suppresses Ovarian Cancer Stem-Cell Proliferation and Stemness

Lee

Kim

Lee

et al. 2020

IJMS

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Epithelial ovarian cancer (EOC) is the most lethal gynecological malignancy in women worldwide, with an overall 5 year survival rate below 30%. The low survival rate is associated with the persistence of cancer stem cells (CSCs) after chemotherapy. Therefore, CSC-targeting strategies are required for successful EOC treatment. Pan-human epidermal growth factor receptor 4 (HER4) and L-type calcium channels are highly expressed in ovarian CSCs, and treatment with the pan-HER inhibitor poziotinib or calcium channel blockers (CCBs) selectively inhibits the growth of ovarian CSCs via distinct molecular mechanisms. In this study, we tested the hypothesis that combination treatment with poziotinib and CCBs can synergistically inhibit the growth of ovarian CSCs. Combined treatment with poziotinib and manidipine (an L-type CCB) synergistically suppressed ovarian CSC sphere formation and viability compared with either drug alone. Moreover, combination treatment synergistically reduced the expression of stemness markers, including CD133, KLF4, and NANOG, and stemness-related signaling molecules, such as phospho-STAT5, phospho-AKT, phospho-ERK, and Wnt/β-catenin. Moreover, poziotinib with manidipine dramatically induced apoptosis in ovarian CSCs. Our results suggest that the combinatorial use of poziotinib with a CCB can effectively inhibit ovarian CSC survival and function.

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“…The activation of mTOR phosphorylates the downstream P70S6K1 effector to initiate the translation process and promote the synthesis of RNA and proteins (24,25). This pathway participates in the occurrence and development of multiple tumors and angiogenesis, and is also considered as the primary pathway for cancer cell survival (26,27). Then, in vitro cell experiment indicated that the transfection with PI3K/AKT/mTOR pathway agonist IGF-1 recovered the pro-apoptotic effects of PTPRZ1 overexpression.…”

Section: Discussionmentioning

confidence: 99%

PTPRZ1 Inhibits the Cisplatin Resistance of Ovarian Cancer by Regulating PI3K/AKT/mTOR Signal Pathway

Wang

et al. 2020

Preprint

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Background: Cisplatin resistance (DDP resistance) is a major cause for poor prognosis of ovarian cancer patients. PTPRZ1 has been proven to participate in the occurrence and development of multiple tumors, including tumor resistance. This study was designed to investigate the roles of PTPRZ1 in DDP-resistant ovarian cancer cells and their possible mechanism.Methods: PTPRZ1 expression in ovarian cancer tissues and normal tissues was analyzed by GEPIA database and verified by qRT-PCR. PTPRZ1 expression in normal ovarian cancer cells and DDP-resistant ovarian cancer cells was also analyzed. Subsequently, qRT-PCR, western blot, MTT experiment and flow cytometry were used to assess the effects of PTPRZ1-PI3K/AKT/mTOR regulating axis on cisplatin resistance of ovarian cancer.Results: PTPRZ1 expression was abnormally low in ovarian cancer tissues, and notably reduced in DDP-resistant ovarian cancer cells. MTT experiment and flow cytometer indicated that overexpression of PTPRZ1 enhanced the cisplatin sensitivity of ovarian cancer cells and promoted the cell apoptosis. The results of mechanism research showed that PTPRZ1 exerted its biological effects possibly through blocking PI3K/AKT/mTOR pathway.Conclusion: PTPRZ1 suppresses the cisplatin resistance of ovarian cancer and induces the cytotoxicity by blocking PI3K/AKT/mTOR pathway.

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RETRACTED ARTICLE: Roles of the PI3K/AKT/mTOR signalling pathways in neurodegenerative diseases and tumours

Cited by 469 publications

References 116 publications

The role of CENPO expression in the progression of non-small cell lung cancer

The role of CENPO expression in the progression of non-small cell lung cancer

Combined Poziotinib with Manidipine Treatment Suppresses Ovarian Cancer Stem-Cell Proliferation and Stemness

PTPRZ1 Inhibits the Cisplatin Resistance of Ovarian Cancer by Regulating PI3K/AKT/mTOR Signal Pathway

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