Cisplatin-mediated down-regulation of miR-145 contributes to up-regulation of PD-L1 via the c-Myc transcription factor in cisplatin-resistant ovarian carcinoma cells

Sheng, Qing; Zhang, Y; Wang, Z; Ding, Jiangwei; Song, Yingfang; Zhao, Wei

doi:10.1111/cei.13406

Cited by 43 publications

(28 citation statements)

References 37 publications

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“…Programmed death‐ligand 1 (PD‐L1) is an inhibitory molecule expressed by cancer cells, which plays a significant role in immune tolerance through the induction of T cell dysfunction. The MiR‐145/c‐Myc/PD‐L1 axis contributed to cisplatin resistance in ovarian cancer 10 …”

Section: Mir‐145 In Drug Resistancementioning

confidence: 99%

“…Researchers are currently attempting to explore the target genes of miR‐145 and their signaling pathways involved in altering therapeutic response, which is significant for the development of miRNA‐related therapies. Strikingly, various research has disclosed that miR‐145 acts in reversion of therapeutic resistance in multiple tumors, including lung cancer, 3‐6 esophageal squamous cell carcinoma (ESCC), 7‐9 ovarian carcinoma, 10,11 glioma, 12,13 hepatocellular carcinoma (HCC), 14‐16 breast cancer, 17 colorectal cancer (CRC) 18‐21 prostate cancer, 22,23 bladder cancer, 24 gastric cancer (GC), 25,26 pancreatic adenocarcinoma 27 and cervical cancer 28,29 …”

Section: Introductionmentioning

confidence: 99%

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MiR‐145 in cancer therapy resistance and sensitivity: A comprehensive review

Hua

Deng

et al. 2020

Cancer Science

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MircoRNA (miRNA) are a group of small, non–coding, regulatory RNA with an average length of approximately 22 nucleotides, which mostly modulate gene expression post–transcriptionally through complementary binding to the 3ʹ‐untranslated region (3ʹ‐UTR) of multiple target genes. Emerging evidence has shown that miRNA are frequently dysregulated in a variety of human malignancies. Among them, microRNA‐145 (miR‐145) has been increasingly identified as a critical suppressor of carcinogenesis and therapeutic resistance. Resistance to tumor therapy is a challenge in cancer treatment due to the daunting range of resistance mechanisms. We reviewed the status quo of recent advancements in the knowledge of the functional role of miR‐145 in therapeutic resistance and the tumor microenvironment. It may serve as an innovative biomarker for therapeutic response and cancer prognosis.

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Section: Mir‐145 In Drug Resistancementioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

MiR‐145 in cancer therapy resistance and sensitivity: A comprehensive review

Hua

Deng

et al. 2020

Cancer Science

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“…22,23 According to earlier studies, miR-145 mostly acts as a tumor suppressor in malignant tumors. 24,25 Our study results demonstrated that miR-145 was lowly expressed in HCC, and was linked to high clinical staging and lymph node metastasis. In addition, follow-up for prognosis revealed that low miR-145 expression was linked to the unfavorable prognosis of the patients.…”

Section: Discussionmentioning

confidence: 70%

<p>MiR-145 Regulates the Chemoresistance of Hepatic Carcinoma Cells Against 5-Fluorouracil by Targeting Toll-Like Receptor 4</p>

Zheng¹,

Ma²,

Li³

et al. 2020

CMAR

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Background: 5-fluorouracil (5-FU) is a common drug for hepatic carcinoma (HCC), but the drug resistance of clinical chemotherapy restricts its use. Studies have demonstrated that miRNA molecules can act as a chemoresistance regulator in drug resistance of tumors, whereas the role of miR-145 in the 5-FU-resistant HCC remains unclear. Objective: To explore the prognostic value of miR-145 in HCC and its molecular mechanism in 5-FU-resistant HCC cells. Methods: A qRT-PCR assay was conducted to quantify miR-145 in HCC tissues and 5-FUresistant HCC cells. The Cell Counting Kit-8 (CCK-8) and flow cytometry were adopted to analyze the proliferation and apoptosis of 5-FU-resistant HCC cells. The Western blot was adopted to quantify toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), and apoptosis-related proteins. Moreover, an in vivo tumor xenotransplantation of nude mice was conducted to determine the effect of miR-145 on 5-FU-resistant HCC cells. Results: MiR-145 was expressed lowly in HCC tissues and cells, and linked to high TNM staging and lymph node metastasis of HCC patients. Down-regulation of miR-145 indicated a poorer prognosis and it promoted drug resistance of HCC cells and inhibited cell apoptosis. In contrast, miR-145 overexpression improved the sensitivity of HCC cells to 5-FU and enhanced the inhibition of 5-FU on tumor growth. The luciferase reporter gene assay showed that TLR4 was the direct target of miR-145, and the Western blot assay revealed that overexpression of TLR4 reversed the inhibitory effect of miR-145 overexpression on TLR4 and MyD88 protein and the effects of it on apoptosis-related proteins. Conclusion: MiR-145 is an inhibiting factor in HCC and can target TLR4 to mediate the chemoresistance of HCC, which may provide novel ideas for treating HCC.

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“…Our observations were consistent with previous studies and confirmed the involvement of TUG1 in the ceRNA mechanism. Notably, there have been several other miRNAs negatively regulated by TUG1 in cancers (60)(61)(62), among which quite a few miRNAs have been reported to have a tumor suppressive role in OC (63)(64)(65). TUG1 could sponge more than one miRNA in OC and affect the development of OC through different signaling pathways.…”

Section: Discussionmentioning

confidence: 99%

miR‑1299/NOTCH3/TUG1 feedback loop contributes to the malignant proliferation of ovarian cancer

Pei

Lou

et al. 2020

Oncol Rep

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Recent studies have revealed the oncogenic role of notch reporter 3 (NOTCH3) in ovarian cancer (OC). However, the possible regulators and mechanisms underlying notch receptor 3 (NOTCH3)-mediated behaviors in OC remain to be completely investigated. In the present study, we aimed to identify regulators of NOTCH3 and their interactions underlying the pathogenesis of OC. Bioinformatics analysis and luciferase reporter assay were used to identify potential regulatory miRNAs and lncRNAs of NOTCH3 in OC. Several in vivo and in vitro assays were performed to evaluate their effects on the proliferative ability mediated by NOTCH3. We identified microRNA-1299 (miR-1299) as a novel negative regulator of NOTCH3. miR-1299 was downregulated in OC and was found to be considerably correlated with tumor differentiation. Upregulation of miR-1299 inhibited cell proliferation, colony formation, and 5-ethynyl-2'-deoxyuridine (EdU) incorporation, as well as induced cell cycle arrest in the G0G1 phase in OC cells. Overexpression of miR-1299 in xenograft mouse models suppressed tumor growth in vivo. The lncRNA taurine upregulated gene 1 (TUG1), acting as a sponge of miR-1299, was found to upregulate NOTCH3 expression and promote cell proliferation in OC through the competing endogenous RNA mechanism. In addition, TUG1 was found to be a potential downstream target of NOTCH3, forming a miR-1299/NOTCH3/TUG1 feedback loop in the development of OC. Collectively, our findings improve the understanding of NOTCH3-mediated regulation in OC pathogenesis and facilitate the development of miRNA-and lncRNA-directed diagnostics and therapeutics against this disease.

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Cisplatin-mediated down-regulation of miR-145 contributes to up-regulation of PD-L1 via the c-Myc transcription factor in cisplatin-resistant ovarian carcinoma cells

Cited by 43 publications

References 37 publications

MiR‐145 in cancer therapy resistance and sensitivity: A comprehensive review

MiR‐145 in cancer therapy resistance and sensitivity: A comprehensive review

<p>MiR-145 Regulates the Chemoresistance of Hepatic Carcinoma Cells Against 5-Fluorouracil by Targeting Toll-Like Receptor 4</p>

miR‑1299/NOTCH3/TUG1 feedback loop contributes to the malignant proliferation of ovarian cancer

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