ANXA6 Contributes to Radioresistance by Promoting Autophagy via Inhibiting the PI3K/AKT/mTOR Signaling Pathway in Nasopharyngeal Carcinoma

Chen, Qianping; Wang, Zheng; Zhu, Lin; Yao, Dan; Wang, Chen; Song, Yimeng; Hu, Songling; Liu, Hongxia; Bai, Yang; Pan, Yan; Zhang, Jianghong; Guan, Jian; Shao, Chunlin

doi:10.3389/fcell.2020.00232

Cited by 32 publications

(26 citation statements)

References 43 publications

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“…The PI3K/AKT/mTOR signaling pathway is involved in cell proliferation, growth, differentiation, and cytoskeletal reorganization in many types of cancer [39][40][41]. Our study showed that the overexpression of miR-124-3p affected tumor progression in NPC cells through the PI3K/AKT/mTOR pathway.…”

Section: Discussionmentioning

confidence: 58%

MicroRNA-124-3p inhibited progression of nasopharyngeal carcinoma by interaction with PCDH8 and the inactivation of PI3K/AKT/mTOR pathway

Ye¹,

Liao²,

Zeng³

et al. 2021

J. Cancer

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Nasopharyngeal carcinoma (NPC) is characterised by distinct geographical distribution and is particularly prevalent in Asian countries. But the mechanisms related to the progression of nasopharyngeal carcinoma (NPC) are not completely understood. MiR-124-3p functions as a tumor suppressor in many kinds of human cancers. Here, we explored the effects and mechanism of miR-124-3p on the proliferation and colony formation in NPC. In our study, we reported that miR-124-3p was significantly downregulated in NPC tissues and cell lines. Overexpression miR-124-3p decreased NPC cell proliferation and colony formation abilities. Meanwhile, knockdown miR-124-3p increased proliferation and colony formation abilities. Additionally, dual-luciferase assay showed that miR-124-3p could positively regulated PCDH8 by targeting its 3'-UTR. Overexpression of PCDH8 could partially rescue the proliferation and colony formation role of miR-124-3p inhibitor. Our study indicated that miR-124-3p played a tumor suppressor by directly interacting with PCDH8 and inhibiting the activation of the phosphatidylinositol 3-kinase (PI3K)/AKT/mammalian target of rapamycin (mTOR) signaling pathway. Overall, we found that miR-124-3p inhibited the activation of the PI3K/AKT/mTOR signaling pathway in NPC by interacting with PCDH8. Thus, PCDH8 may be a potential molecular target that impeded NPC proliferation and colony formation.

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Section: Discussionmentioning

confidence: 58%

MicroRNA-124-3p inhibited progression of nasopharyngeal carcinoma by interaction with PCDH8 and the inactivation of PI3K/AKT/mTOR pathway

Ye¹,

Liao²,

Zeng³

et al. 2021

J. Cancer

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“…Among these seven IAGs, ANXA6 can regulate IL-2 homeostasis and sensitivity in T cells [19] and has been demonstrated that was correlated with the development of cancers, such as breast cancer and pancreatic cancer [20,21]. Chen et al showed that ANXA6 could enhance the radioresistance of nasopharyngeal carcinoma by inhibiting PI3K/AKT/mTOR signalling pathway [22]. AHNAK, a large structural scaffold protein, has been proven to be a prognostic biomarker in pancreatic ductal adenocarcinoma, glioma, as well as BC [23][24][25].…”

Section: Discussionmentioning

confidence: 99%

Construction of a immune-associated genes based prognostic signature in bladder cancer

Shen

Wang

Yang

et al. 2021

Artificial Cells, Nanomedicine, and Biotechnology

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Current studies indicated that immune-associated genes (IAGs) have important roles in the occurrence and development of bladder cancer (BC). The current work aims to identify the prognostic values of IAGs in BC and establish a prognostic signature based on IAGs. RNA sequencing data and protein expression data were used to identify differentially expressed IAGs in BC. An IAGs based signature was further constructed and the prognostic and predictive values of the signature were evaluated by survival analysis and nomogram. RNA isolation and reverse transcription-quantitative PCR (RT-qPCR) were further performed to investigate the expression levels of IAGs in BC cells and were used to explore the relationship between IAGs and M2 tumour-associated macrophages (TAMs) secreted transforming growth factor-b1 (TGF-b1) in BC cells. We selected five IAGs to develop an IAGs signature model, which were significantly related to survival outcomes of BC patients. RT-qPCR showed that five IAGs were significantly differentially expressed and three IAGs were positively correlated with M2 TAMs secreted TGF-b1 in T24 cells. We identified and validated an IAGs based signature to predict the prognosis of BC patients. Furthermore, M2 TAMs may promote the expression of IAGs in BC via the TGF-b1 signalling pathway.

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“…MicroRNA-493-5p suppresses colorectal cancer progression via the PI3K-Akt-FoxO3a signaling pathway (69). ANXA6 contributes to radioresistance by promoting autophagy via inhibiting the PI3K/AKT/mTOR signaling pathway in nasopharyngeal carcinoma (70). Recently, 4E-BP1 was shown to be phosphorylated by other kinases besides mTOR, and overexpression of 4E-BP1 was found in different human carcinomas (71).…”

Section: Discussionmentioning

confidence: 99%

miR155 Enhances Autophagy by Reducing MBD5 and METTL3 in Human Liver Cancer Stem Cells

Lu¹,

Chen²,

Xin³

et al. 2020

Preprint

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Background: miR-155 is a widely reported carcinogenic miRNA, with up-regulated expression in a variety of human cancers. Methods: Liver cancer stem cells were isolated from Huh7 cells; gene infection, RT-PCR, Western blotting and tumorigenesis test in vitro and in vivo were performed to analyze the signaling pathway. Results: we demonstrate that miR-155 inhibits the expression of MBD5 and METTL3 , reducing the expression of DNMT1. In particular, miR155 inhibits the interaction between MBD5 and DNMT1, thereby inhibiting the binding capacity among MBD5, DNMT1 and IGFII (H19 ICR, IGFII DMR, IGFII Enhancer) DNA, inhibiting IGFII DNA methylation modification. Importantly, miR-155 promotes the formation of DNA loops in the IGFII DNA region (H19 ICR-IGFII Enhancer, IGFII DMR-IGFII Enhancer). Therefore, miR155 promotes the binding ability of H19-pre miR675 to histone methyltransferases SUV39h2 dependent on the H19 ICR-IGFII enhancer DNA loop and enhances the methylation modification of histone H3 on the ninth lysine . Then, the binding ability of RNA polII to P300 was enhanced by the formation of H3K9me2-RNA polII-P300 complex. Furthermore, miR155 promotes the binding ability of the RNA PolII-P300 complex to the IGFII promoter dependent on the IGFII DMR-IGFII enhancer DNA loop and promotes the expression of IGFII. Further research shows that miR155 promotes the binding of IGFII to stemness factors and the loading of stemness factors into the promoter region of HGF, which promotes the expression of hepatocyte growth factor HGF. In particular, miR155 promotes the expression of albumin gene (ALB) via HGF-c-MET, and then promotes the Sirt1 expression through ALB. Strikingly, miR155 promotes the autophagy dependent on acetylase Sirt1,including that miR155 promotes LC3 activation dependent on acetylase sirt1 and enhances binding capacity of LC3 to TP53INP2 / DOR, ATG4, ATG3 and ATG7, and the binding ability of the interaction between ATG5, ATG12, ATG6L1, ATG9. More meaningfully, miR155 enhances the ability of H-Ras to bind to the autophagosomes Beclin1, vps34, vps5, Uvrage, bif1, Lamp1, Lamp2, Lamp3, Rubicon, Rab24 dependent on autophagy, thereby enhancing the expression of H-Ras. Furthermore, miR155 enhances the expression of pRaf1, pMEK1 / 2, pERK1 / 2, pElK, pJak, Jun, pAKT, pmTOR, P70S6K, 4E-BP1, SGK1, C-myc dependent on H-Ras.Finally, miR-155 promotes the malignant growth of human liver cancer stem cells mediated by H-Ras.Conclusions: these results provide a valuable theoretical basis for therapeutic targets of liver cancer based on miR-155.

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ANXA6 Contributes to Radioresistance by Promoting Autophagy via Inhibiting the PI3K/AKT/mTOR Signaling Pathway in Nasopharyngeal Carcinoma

Cited by 32 publications

References 43 publications

MicroRNA-124-3p inhibited progression of nasopharyngeal carcinoma by interaction with PCDH8 and the inactivation of PI3K/AKT/mTOR pathway

MicroRNA-124-3p inhibited progression of nasopharyngeal carcinoma by interaction with PCDH8 and the inactivation of PI3K/AKT/mTOR pathway

Construction of a immune-associated genes based prognostic signature in bladder cancer

miR155 Enhances Autophagy by Reducing MBD5 and METTL3 in Human Liver Cancer Stem Cells

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