LincRNA-RoR/miR-145 promote invasion and metastasis in triple-negative breast cancer via targeting MUC1

Ma, Jianying; Yang, Yue; Huo, Desheng; Wang, Zanyu; Zhai, Xiaoyu; Chen, Jing; Sun, Hongwei; An, Wei; Jie, Jing; Yang, Pengxiang

doi:10.1016/j.bbrc.2018.04.119

Cited by 38 publications

(38 citation statements)

References 26 publications

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“…Other work revealed MUC1 to be part of a miR-322-dependent regulatory loop in human carcinomas (33). In accordance with the present results, a previous study demonstrated that LincRNA-RoR/miR-145 accelerated the invasion and metastasis of triple negative breast cancer by up-regulating expression of MUC1 (34). Further, it has been suggested that miR-128 may serve as an attractive therapeutic strategy for paclitaxel-resistant lung cancer via inhibition of MUC1-C (35).…”

Section: Discussionsupporting

confidence: 93%

Methylation-Mediated Silencing of MicroRNA-497 Promotes Breast Cancer Progression Through Up-Regulation of Mucin1

Tao

et al. 2020

Front. Oncol.

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Background: Potential anti-tumor effects of microRNA-497 (miR-497) have been highlighted in various malignancies including breast cancer. However, little is known about the function of miR-497 and its putative target mucin1 (MUC1) in breast cancer. The present study explored how miR-497 regulates breast cancer progression in a MUC1-dependent manner. Methods: Expression of miR-497 and MUC1 was determined in breast cancer tissues and cells. Methylation specific polymerase chain reaction was used to measure the methylation status of CpG islands of miR-497 promoter, while chromatin immunoprecipitation assay was used to detect recruitment of methyltransferase to the promoter region of miR-497. Alteration in expression of miR-497 (overexpression) and MUC1 (up-and down-regulation) was performed to examine their roles in breast cancer biology in vitro and in vivo. The binding affinity between miR-497 and MUC1 was investigated through a bioinformatics database and dual luciferase reporter gene assay. Results: MiR-497 was down-regulated and MUC1 was up-regulated in breast cancer tissues and cell lines. Besides, methylation induced a down-regulation of miR-497 in breast cancer. The bioinformatics analysis and dual luciferase reporter gene assay indicated that miR-497 targeted MUC1. Overexpression of miR-497 inhibited breast cancer cell proliferation and invasion and promoted the apoptosis of breast cancer cells by down-regulating MUC1. The inhibitory action of miR-497 on tumor growth was validated in vivo. Conclusion: In conclusion, miR-497 down-regulated MUC1 expression and subsequently suppressed breast cancer progression, highlighting miR-497 to be a potential biomarker and therapeutic target for breast cancer therapy.

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Section: Discussionsupporting

confidence: 93%

Methylation-Mediated Silencing of MicroRNA-497 Promotes Breast Cancer Progression Through Up-Regulation of Mucin1

Tao

et al. 2020

Front. Oncol.

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“…MicroRNAs (miRNAs) are closely related to tumors and regulate the progression of the tumor (Ma et al, 2018;Xie, Liang, Su, An, & Qu, 2018;Yu et al, 2018;Zhou, Xia, Su, & Zhang, 2014). miR-145 has been shown to be downregulated in many cancers (Chan et al, 2013;Cho, Chow, & Au, 2011;Gramantieri et al, 2009;Kim et al, 2015;Shi et al, 2007;Xu et al, 2012); it regulates biological functions of cancer cells through target gene (Sachdeva & Mo, 2010;Sachdeva et al, 2009;Zhang et al, 2010;Zhang et al, 2011).…”

Section: Introductionmentioning

confidence: 99%

miR‐145 promotes miR‐133b expression through c‐myc and DNMT3A‐mediated methylation in ovarian cancer cells

Zhang

Zou

et al. 2019

Journal Cellular Physiology

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Ovarian cancer presents as malignant tumors in the female reproductive system with high mortality. MicroRNAs are involved in the progression of ovarian cancer; however, the regulatory relationship among miRs remains unclear. In our study, we verified that both miR-145 and miR-133b messenger RNA (mRNA) levels in ovarian cancer tissues were lower than in normal ovarian tissues, and their mRNA level in serum of patients with ovarian cancer was reduced. We demonstrated miR-145 targeted c-myc, and c-myc interacted physically with DNMT3A in ovarian cancer cells. We confirmed that c-myc recruited DNMT3A to the miR-133b promoter. miR-133b overexpression also inhibited target gene PKM2 expression along with the Warburg effect. Our results indicate that miR-145 inhibited the Warburg effect through miR-133b/PKM2 pathways, which may improve approaches to ovarian cancer diagnosis and treatment. K E Y W O R D Sc-myc, DNMT3A, miR-133b, miR-145, ovarian cancer, Warburg effect

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“…Furthermore, the miR-181a was involved in TNBC metastasis via elevated expression of Bim [72]. [115,116] miR-373 TXNIP Induces cancer cell EMT and metastasis [117,118] miR-10b HOXD10 Promotes invasion and metastasis [119] miR-21 PTEN Lymph node metastasis [120] miR-17/92 cluster COL4A3, LAMA3, TIMP2/3 Lymph node metastases, promote metastasis [121,122] miR-629-3p LIFR Lung metastases [123] miR-455-3p EI24 Promotes proliferation, invasion, and migration [124] miR-125b APC Promotes proliferation, metastasis, and EMT [125] miR-181a Bim Promotes EMT, migratory, and invasive [72] Oncosuppressor miRNAs miR-200a/b/c PKCα, UBASH3B, XIAP Suppress proliferation, migration, invasion, and metastasis, promote apoptosis [77,126,127] miR-205 Unknown Lymph node metastasis [128] let-7 RAS, c-Myc Block growth and reduce metastasis [129] miR-145 MUC1, Arf6, JAM-A, Fascin Reduce cell motility, invasiveness, and metastasis [130][131][132] miR-206 CORO1C Regulates metastasis [133] miR-30a ROR1 Associates with high histological grade and more lymph node metastasis [134] miR-190a/940 Unknown Prevents metastasis and cell invasion [19,135] miR-33b HMGA2, SALL4, Twist1 Inhibit metastasis [114] miR-146a-5p SOX5 Inhibits proliferation and metastasis [136] miR-150 HMGA2 Inhibits metastasis [137] miR-124 ZEB2 Inhibits invasion and metastasis [138] miR-148a WNT1, NRP1 Suppress metastasis [139] miR-126-3p RGS3 Inhibits proliferation, migration, invasion, and angiogenesis [140] miR-508-3p ZEB1 Inhibits cell invasion and EMT [141] miR-613 Daam1 Inhibits cell migration and invasion [142] miR-519d-3p LIMK1 Suppresses growth and mot...…”

Section: Mirnas In Regulation Of Metastasis In Tnbcmentioning

confidence: 99%

“…A report by Aceto et al indicated that Src-homology 2 domain-containing phosphatase 2 (SHP2) activated the ERKs, causing upregulation of ZEB1, as well as v-myc myelocytomatosis viral oncogene homolog (c-Myc), which resulted in the repression of let-7 miRNA and increased the expression of let-7 targets, including RAS and c-Myc, forming a key positive feedback signaling loop involved in the TNBC progression [129]. Ma et al showed that large intergenic ncRNA-regulator of reprogramming (lincRNA-ROR) functions as a competing endogenous RNA (ceRNA) that sponges miR-145 and upregulates the expression of mucin1 (MUC1) to promote invasion and metastasis in TNBC [130]. MiR-145 was shown to regulate invasion and metastasis in TNBC by targeting small GTPase ADP-ribosylation factor 6 (Arf6) to affect E-cadherin localization and impact cell-cell adhesion [131].…”

Section: Mirnas In Regulation Of Metastasis In Tnbcmentioning

confidence: 99%

MicroRNAs Involved in Carcinogenesis, Prognosis, Therapeutic Resistance, and Applications in Human Triple-Negative Breast Cancer

Ding

Xiong

et al. 2019

Cells

115

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Triple-negative breast cancer (TNBC) is the most aggressive, prevalent, and distinct subtype of breast cancer characterized by high recurrence rates and poor clinical prognosis, devoid of both predictive markers and potential therapeutic targets. MicroRNAs (miRNA/miR) are a family of small, endogenous, non-coding, single-stranded regulatory RNAs that bind to the 3′-untranslated region (3′-UTR) complementary sequences and downregulate the translation of target mRNAs as post-transcriptional regulators. Dysregulation miRNAs are involved in broad spectrum cellular processes of TNBC, exerting their function as oncogenes or tumor suppressors depending on their cellular target involved in tumor initiation, promotion, malignant conversion, and metastasis. In this review, we emphasize on masses of miRNAs that act as oncogenes or tumor suppressors involved in epithelial–mesenchymal transition (EMT), maintenance of stemness, tumor invasion and metastasis, cell proliferation, and apoptosis. We also discuss miRNAs as the targets or as the regulators of dysregulation epigenetic modulation in the carcinogenesis process of TNBC. Furthermore, we show that miRNAs used as potential classification, prognostic, chemotherapy and radiotherapy resistance markers in TNBC. Finally, we present the perspective on miRNA therapeutics with mimics or antagonists, and focus on the challenges of miRNA therapy. This study offers an insight into the role of miRNA in pathology progression of TNBC.

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LincRNA-RoR/miR-145 promote invasion and metastasis in triple-negative breast cancer via targeting MUC1

Cited by 38 publications

References 26 publications

Methylation-Mediated Silencing of MicroRNA-497 Promotes Breast Cancer Progression Through Up-Regulation of Mucin1

Methylation-Mediated Silencing of MicroRNA-497 Promotes Breast Cancer Progression Through Up-Regulation of Mucin1

miR‐145 promotes miR‐133b expression through c‐myc and DNMT3A‐mediated methylation in ovarian cancer cells

MicroRNAs Involved in Carcinogenesis, Prognosis, Therapeutic Resistance, and Applications in Human Triple-Negative Breast Cancer

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