PU.1/microRNA-142-3p targets ATG5/ATG16L1 to inactivate autophagy and sensitize hepatocellular carcinoma cells to sorafenib

Zhang, Kai; Chen, Jing; Zhou, Hao; Chen, Ying; Zhi, Yingru; Zhang, Bei; Chen, Longbang; Chen, Xiaoyuan; Wang, Rui; Zhang, Chenyu

doi:10.1038/s41419-018-0344-0

Cited by 93 publications

(59 citation statements)

References 44 publications

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“…The expressions of hsa-miR-125a-5p, hsa-miR-107, hsa-miR-17-5p and hsa-miR-22-3p in HCC were consistent with published studies [30][31][32][33]. However, several studies have come up with results that were ambivalent with ours in hsa-miR-216b-5p, hsa-miR-142-3p and hsa-miR-20b-5p [34][35][36]. Since the heterogeneity of cross-studies cannot be ignored and the credibility of the combined results may decrease due to interfusion of the low-quality studies, more studies are needed to verify these results.…”

Section: Discussionsupporting

confidence: 90%

Role of FBXL19-AS1 in hepatocellular carcinoma by lncRNA–miRNA–mRNA network analysis and its diagnostic and prognostic value

Zhang

Zhu

et al. 2020

Preprint

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Background: Hepatocellular carcinoma (HCC) is one of the most common neoplastic diseases worldwide. Available biomarkers are not sensitive enough for the diagnosis of HCC, seeking new biomarkers of HCC is urgent and challenging. The purpose of this study was to investigate the role of F-box and leucine-rich repeat protein 19-antisense RNA 1 (FBXL19-AS1) through competing endogenous RNA (ceRNA) network and its diagnostic and prognostic value in HCC.Methods: A comprehensive strategy of genomic data mining, bioinformatics and experimental validation was used to evaluate the clinical value of FBXL19-AS1 in the diagnosis and prognosis of HCC and to identify the pathways that FBXL19-AS1 may be involved in.Results: FBXL19-AS1 was up-regulated in HCC, and its high expression was associated with TNM stage and poor prognosis of HCC patients. The combined use of plasma FBXL19-AS1 and alpha-fetoprotein (AFP) could prominently improve the diagnostic validity for HCC. FBXL19-AS1 might participate in regulating HCC related pathways, including hepatitis C, hepatitis B, microRNAs in cancer, cell cycle, viral carcinogenesis, and proteoglycans in cancer through ceRNA network.Conclusions: Our findings indicated that FBXL19-AS1 not only serves as a potential biomarker for HCC diagnosis and prognosis, but it may be functionally carcinogenic.

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Section: Discussionsupporting

confidence: 90%

Role of FBXL19-AS1 in hepatocellular carcinoma by lncRNA–miRNA–mRNA network analysis and its diagnostic and prognostic value

Zhang

Zhu

et al. 2020

Preprint

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“…Therefore, a search for potential target genes of miR-874 in GC using several computational algorithms was performed. Among the potential targets, ATG16L1 was focused on as its function is associated with chemoresistance in cancer (29). The results of the present study revealed that the expression of ATG16L1 was increased in drug-resistant GC cells.…”

Section: Discussionmentioning

confidence: 64%

miR-874 regulates multiple-drug resistance in gastric cancer by targeting ATG16L1

Huang¹,

Tang

Zhang

et al. 2018

Int J Oncol

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Chemotherapy is an important treatment option for gastric cancer (GC); however, chemotherapy usually fails due to drug resistance, particularly multidrug resistance (MDR). In our previous studies, microRNA (miR)-874 was demonstrated to serve an important role in tumour growth, apoptosis and angiogenesis. In the present study, the precise roles and underlying mechanisms of miR-874 in MDR were investigated in GC. The overexpression of miR-874 reversed cancer cell drug resistance in vitro. According to reporter gene and western blot assays, Autophagy-related 16-like 1 (ATG16 L1) was identified as a direct target of miR-874. ATG16L1 was also demonstrated to be positively associated with autophagy. Reducing the expression of ATG16L1 and inhibiting the occurrence of autophagy sensitized GC cells to chemotherapy. Thus, the miR-874/ATG16L1/autophagy regulatory loop was demonstrated to serve an important role in MDR in GC. Furthermore, miR-874 may be used as a prognostic factor in GC. Overall, miR-874 could inhibit autophagy and sensitize GC cells to chemotherapy via the target gene ATG16L1, highlighting the potential clinical application of miR-874 in chemotherapeutic resistance.

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“…The ability of these miRNAs to restrain autophagy contributes to the sensitization of cancer cells to anti-cancer agents [95,97,100]. In addition to ATG5, the inhibitory effects of miR-142-3p on therapeutic resistance can be mediated by targeting ATG16L1 [97]. Moreover, a recent study also indicated that autophagy inhibition in miR-874-3p over-expressing cells abrogates therapeutic resistance [104] (Table 3).…”

Section: Mirnas Regulating the Lipidation Of Lc3mentioning

confidence: 99%

“…ATG5 can be targeted by multiple miRNAs, including miR-137-3p, miR-142-3p, and miR-224-3p. The ability of these miRNAs to restrain autophagy contributes to the sensitization of cancer cells to anti-cancer agents [95,97,100]. In addition to ATG5, the inhibitory effects of miR-142-3p on therapeutic resistance can be mediated by targeting ATG16L1 [97].…”

Section: Mirnas Regulating the Lipidation Of Lc3mentioning

confidence: 99%

MicroRNA-Based Combinatorial Cancer Therapy: Effects of MicroRNAs on the Efficacy of Anti-Cancer Therapies

Seo

Moeng

Sim³

et al. 2019

Cells

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The susceptibility of cancer cells to different types of treatments can be restricted by intrinsic and acquired therapeutic resistance, leading to the failure of cancer regression and remission. To overcome this problem, a combination therapy has been proposed as a fundamental strategy to improve therapeutic responses; however, resistance is still unavoidable. MicroRNA (miRNAs) are associated with cancer therapeutic resistance. The modulation of dysregulated miRNA levels through miRNA-based therapy comprising a replacement or inhibition approach has been proposed to sensitize cancer cells to other anti-cancer therapies. The combination of miRNA-based therapy with other anti-cancer therapies (miRNA-based combinatorial cancer therapy) is attractive, due to the ability of miRNAs to target multiple genes associated with the signaling pathways controlling therapeutic resistance. In this article, we present an overview of recent findings on the role of therapeutic resistance-related miRNAs in different types of cancer. We review the feasibility of utilizing dysregulated miRNAs in cancer cells and extracellular vesicles as potential candidates for miRNA-based combinatorial cancer therapy. We also discuss innate properties of miRNAs that need to be considered for more effective combinatorial cancer therapy.Cells 2020, 9, 29 2 of 32 to confer the ability to acquire CSC properties onto cancer cells, thereby contributing to therapeutic resistance [7]. Moreover, cell-to-cell communication via extracellular vesicles among different types of cells within the cancer microenvironment could affect the efficacy of cancer therapies by delivering miRNAs that regulate various signaling pathways connected to therapeutic resistance [8,9].Combination therapies have been proposed to overcome therapeutic resistance via the combined inhibition of different mechanisms. For example, the combination of cobimetinib and pictilisib was reported to be beneficial for the treatment of colorectal cancer cells. However, resistance is unavoidable even after the combination treatment [10]. Similarly, the simultaneous inhibition of phosphoinositide 3-kinase (PI3K) and a mechanistic target of rapamycin kinase (mTOR) was reported to activate extracellular signal-regulated kinase (ERK), a pro-survival factor, in acute myeloid leukemia [11]. Therefore, it is still necessary to explore new combination strategies to defeat therapeutic resistance. An improved understanding of the cellular basis of cancer therapeutic resistance can further provide promising opportunities to design and develop novel cancer treatment strategies to manage cancers.MicroRNAs (miRNAs) are widely recognized, small, regulatory RNAs modulating numerous intracellular signaling pathways in several diseases, including cancers. Based on the expression levels and intracellular functions of miRNAs, they could act as tumor-suppressive or oncogenic factors in cancer cells [12][13][14]. The abnormal expression of miRNAs is associated with therapeutic resistance in cancer, and the modulation of m...

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PU.1/microRNA-142-3p targets ATG5/ATG16L1 to inactivate autophagy and sensitize hepatocellular carcinoma cells to sorafenib

Cited by 93 publications

References 44 publications

Role of FBXL19-AS1 in hepatocellular carcinoma by lncRNA–miRNA–mRNA network analysis and its diagnostic and prognostic value

Role of FBXL19-AS1 in hepatocellular carcinoma by lncRNA–miRNA–mRNA network analysis and its diagnostic and prognostic value

miR-874 regulates multiple-drug resistance in gastric cancer by targeting ATG16L1

MicroRNA-Based Combinatorial Cancer Therapy: Effects of MicroRNAs on the Efficacy of Anti-Cancer Therapies

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