The lncRNA XIST/miR‐125b‐2‐3p axis modulates cell proliferation and chemotherapeutic sensitivity via targeting Wee1 in colorectal cancer

Zeng, Zhao-Lei; Lu, Jiahuan; Wang, Yun; Sheng, Hui; Wang, Yingnan; Chen, Zhan-Hong; Wu, Qi‐Nian; Zheng, Jia-Bo; Chen, Yan‐Xing; Yang, Dongdong; Yu, Kai; Mo, Hai-Yu; Hu, Jiajia; Hu, Pei-Shan; Liu, Zexian; Ju, Huai-Qiang; Xu, Rui‐Hua

doi:10.1002/cam4.3777

Cited by 26 publications

(16 citation statements)

References 42 publications

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“…For example, a high level of ENSG00000254615 was related to the repression of tumor growth and the inhibition of 5-FU resistance in CRC [23]. XIST enhanced the chemoresistance and tumorigenesis of CRC by adsorbing miR-125b-2-3p and elevating WEE1 [24]. Previous studies reported that SNHG11 acted as a contributor in triple-negative breast cancer [25], hepatocellular carcinoma [26] and pancreatic carcinoma [27] through different pathways.…”

Section: Discussionmentioning

confidence: 99%

LncRNA SNHG11 enhances bevacizumab resistance in colorectal cancer by mediating miR-1207-5p/ABCC1 axis

et al. 2022

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Long noncoding RNAs (lncRNAs) have been reported to serve as vital regulators in the chemoresistance of human cancers, including colorectal cancer (CRC). In this study, we aimed to explore the functions of lncRNA small nucleolar RNA host gene 11 (SNHG11) in the resistance of CRC to bevacizumab. Quantitative real-time PCR, western blot assay or immunohistochemistry assay were performed to examine the expression of SNHG11, microRNA-1207-5p (miR-1207-5p), ATP binding cassette subfamily C member 1 (ABCC1) and Ki67. Cell Counting Kit-8 assay was conducted to evaluate bevacizumab resistance and cell viability. 5′-ethynyl-2′-deoxyuridine analysis, flow cytometry analysis and wound-healing assay were conducted for cell proliferation, apoptosis and migration, respectively. Dual-luciferase reporter assay and RNA immunoprecipitation assay were employed to analyze the relations among SNHG11, miR-1207-5p and ABCC1. Murine xenograft model assay was employed to analyze bevacizumab resistance in vivo. The exosomes were observed under transmission electron microscopy. SNHG11 was overexpressed in bevacizumab-resistant CRC tissues and cells. Knockdown of SNHG11 restrained bevacizumab resistance, repressed cell proliferation and migration, and promoted apoptosis in bevacizumab-resistant CRC cells. MiR-1207-5p served as the target of SNHG11 and SNHG11 regulated bevacizumab resistance by targeting miR-1207-5p. ABCC1 was the target gene of miR-1207-5p. Overexpression of miR-1207-5p inhibited bevacizumab resistance and cell progression in bevacizumab-resistant CRC cells, with ABCC1 elevation abrogated the impacts. SNHG11 silencing repressed bevacizumab resistance in vivo. In addition, exosomal SNHG11 was upregulated in bevacizumab-resistant CRC cells. SNHG11 contributes to bevacizumab resistance in CRC depending on the modulation of miR-1207-5p and ABCC1.

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Section: Discussionmentioning

confidence: 99%

LncRNA SNHG11 enhances bevacizumab resistance in colorectal cancer by mediating miR-1207-5p/ABCC1 axis

et al. 2022

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“…However, in contrast to our study, the expression of miR-125b-2-3p was rather decreased in other types of cancer. In colorectal cancer, tissue and cell line expression of this miR was decreased, and overexpression increased sensitivity to drugs [ 65 ]. In a similar way, miR-125b-2-3p was significantly lower in HCC than in non-tumor tissue [ 66 ].…”

Section: Discussionmentioning

confidence: 99%

The Profile of MicroRNA Expression and Potential Role in the Regulation of Drug-Resistant Genes in Doxorubicin and Topotecan Resistant Ovarian Cancer Cell Lines

Stasiak

Kaźmierczak

Jopek

et al. 2022

IJMS

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Epithelial ovarian cancer has the highest mortality among all gynecological malignancies. The main reasons for high mortality are late diagnosis and development of resistance to chemotherapy. Resistance to chemotherapeutic drugs can result from altered expression of drug-resistance genes regulated by miRNA. The main goal of our study was to detect differences in miRNA expression levels in two doxorubicin (DOX)- and two topotecan (TOP)-resistant variants of the A2780 drug-sensitive ovarian cancer cell line by miRNA microarray. The next aim was to recognize miRNAs as factors responsible for the regulation of drug-resistance genes. We observed altered expression of 28 miRNA that may be related to drug resistance. The upregulation of miR-125b-5p and miR-935 and downregulation of miR-218-5p was observed in both DOX-resistant cell lines. In both TOP-resistant cell lines, we noted the overexpression of miR-99a-5p, miR-100-5p, miR-125b-5p, and miR-125b-2-3p and decreased expression of miR-551b-3p, miR-551b-5p, and miR-383-5p. Analysis of the targets suggested that expression of important drug-resistant genes such as the collagen type I alpha 2 chain (COL1A2), protein Tyrosine Phosphatase Receptor Type K (PTPRK), receptor tyrosine kinase—EPHA7, Roundabout Guidance Receptor 2 (ROBO2), myristoylated alanine-rich C-kinase substrate (MARCK), and the ATP-binding cassette subfamily G member 2 (ABCG2) can be regulated by miRNA.

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“…133 In addition, XIST can activate the Wnt/β-catenin signaling pathway to accelerate bladder and colon cancer progression by sponging miR-139-5p 105 and miR-34a 109 respectively. XIST targets miR-200b-3p to modulate the expression of ZEB1 , 134 sponges miR-132-3p to activate the MAPK1 signaling pathway, 110 interacts with miR-137 to regulate the EZH2 signaling pathway, 117 binds miR-486-5p to regulate the neuropilin-2 (NRP-2) pathway, 108 inhibits miR-30a-5p to activate ROR1, 135 suppresses miR-93-5p to modulate the HIF-1A/AXL signaling pathway, 136 sponges miR-338-3p to regulate PAX5 expression, 137 and targets miR-125b-2-3p to regulate the Wee1 signaling pathway, 138 all of which promote colorectal cancer progression. XIST can also promote TGF-β-induced epithelial–mesenchymal transition through the miR-367/141-ZEB2 120 and miR-137/Notch-1 124 axes in non-small cell lung cancer.…”

Section: Xist and Sex-biased Diseasesmentioning

confidence: 99%

Long noncoding RNA XIST: Mechanisms for X chromosome inactivation, roles in sex-biased diseases, and therapeutic opportunities

Zhe

Yang

et al. 2022

Genes & Diseases

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The lncRNA XIST/miR‐125b‐2‐3p axis modulates cell proliferation and chemotherapeutic sensitivity via targeting Wee1 in colorectal cancer

Abstract: This is an open access article under the terms of the Creative Commons Attribution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 26 publications

References 42 publications

LncRNA SNHG11 enhances bevacizumab resistance in colorectal cancer by mediating miR-1207-5p/ABCC1 axis

LncRNA SNHG11 enhances bevacizumab resistance in colorectal cancer by mediating miR-1207-5p/ABCC1 axis

The Profile of MicroRNA Expression and Potential Role in the Regulation of Drug-Resistant Genes in Doxorubicin and Topotecan Resistant Ovarian Cancer Cell Lines

Long noncoding RNA XIST: Mechanisms for X chromosome inactivation, roles in sex-biased diseases, and therapeutic opportunities

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