MicroRNAs Involved in Inflammatory Breast Cancer: Oncogene and Tumor Suppressors with Possible Targets

Rezaei, Zohreh; Sadri, Farzad

doi:10.1089/dna.2020.6320

Cited by 8 publications

(5 citation statements)

References 128 publications

(129 reference statements)

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“…miRNAs can promote the growth, proliferation, metastasis, and invasion of tumors and play the role of tumor growth factors. Researchers call this kind of tumor-inducing miRNAs cancer-promoting genes, whereas the miRNAs that exert tumor-inhibiting effects are called tumor suppressor genes [ 18 , 19 ]. Studies have shown that miR-let-7 inhibits the occurrence of a variety of cancers, such as breast cancer [ 20 ], bladder cancer [ 21 ], and colon cancer [ 22 ].…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-let-7 Targets HMGA2 to Regulate the Proliferation, Migration, and Invasion of Colon Cancer Cell HCT116

Chen

Liu

2021

Evidence-Based Complementary and Alternative Medicine

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Objective. To investigate the effect of microRNA-let-7 (miR-let-7) on the proliferation, migration, and invasion of colon cancer cell HCT116 in vitro and its regulatory mechanism on downstream HMGA2. Methods. It was planned to synthesize miR-let-7 overexpression (mimics) and interference expression (inhibitor) and transiently transfect colon cancer cell HCT116, detect the expression levels of miR-let-7 and HMGA2 in the cells after transfection and the targeted regulation effect of miR-let-7 on HMGA2, then detect the effect of upregulation/downregulation of miR-let-7 on HMGA2, and detect the proliferation, migration, and invasion of HCT116 cells. Results. The expression of miR-let-7 was downregulated, and the expression of HMGA2 was upregulated in HCT116. The expression of miR-let-7 increased significantly after HCT116 was transfected with miR-let-7 mimics. The expression of miR-let-7 decreased significantly after HCT116 was transfected with miR-let-7 inhibitor. The bioinformatics websites predicted that miR-let-7 has a binding site with HMGA2, and the dual-luciferase reporter gene experiment detected that miR-let-7 has a targeting relationship with HMGA2. The expression of HMGA2 decreased after HCT116 was transfected with miR-let-7 mimics; the expression of HMGA2 increased after HCT116 was transfected with miR-let-7 inhibitor. After upregulating miR-let-7, the proliferation, migration, and invasion ability of HCT116 was weakened. After miR-let-7 was inhibited, the proliferation, migration, and invasion ability of HCT116 was enhanced. Conclusion. Abnormal expression of miR-let-7 is an important factor affecting the proliferation, migration, and invasion of HCT116 cells, and it can promote or inhibit the biological behavior of cancer cells by targeting the expression of HMGA2. This study provides ideas for the drug development of new gene targets.

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Section: Discussionmentioning

confidence: 99%

MicroRNA-let-7 Targets HMGA2 to Regulate the Proliferation, Migration, and Invasion of Colon Cancer Cell HCT116

Chen

Liu

2021

Evidence-Based Complementary and Alternative Medicine

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“…microRNAs (miRNAs) are small (20–24 nt) non-coding RNAs that are contributed in post-transcriptional regulation of gene expression in multicellular organisms by affecting both the permanency and translation of mRNAs 13 . According to their target genes and the tissues in which they are expressed, miRNAs are classified into different groups such as oncomiRs and tumor suppressors 14 . Specific miRNAs have been found in various cancers having a strong impact on the development of human tumors and the prognosis of patients and abnormal miRNA expression has been identified in a variety of cancers 15 , implying miRNAs as a possible therapeutic target for cancer care 16 .…”

Section: Introductionmentioning

confidence: 99%

EZH2 regulates oncomiR-200c and EMT markers in esophageal squamous cell carcinomas

Nourmohammadi

Forghanifard

Abbaszadegan

et al. 2022

Sci Rep

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EZH2, as a histone methyltransferase, has been associated with cancer development and metastasis possibly through the regulation of microRNAs and cellular pathways such as EMT. In this study, the effect of EZH2 expression on miR-200c and important genes of the EMT pathway was investigated in esophageal squamous cell carcinoma (ESCC). Comparative qRT-PCR was used to examine EZH2 expression in ESCC lines (YM-1 and KYSE‐30) following the separately transfected silencing and ectopic expressional EZH2 vectors in ESCC. Subsequently, expression of miR-200c and EMT markers was also assessed using qRT-PCR, western blotting and immunocytochemistry. Underexpression of Mir200c was detected in YM-1 and KYSE-30 cells after EZH2 silencing, while its overexpression was observed after EZH2 induced expression. Following EZH2 silencing, downregulation of mesenchymal markers and upregulation of epithelial markers were detected in the ESCCs. Our results demonstrate that EZH2 regulates the expression of miR-200c and critical EMT genes, implying that overexpression of Zeb2, Fibronectin, N-cadherin, and Vimentin lead to a mesenchymal phenotype and morphology while underexpression of epithelial genes, enhance cell migration after enforced expression of EZH2 in ESCCs. EZH2 gene can be a beneficial treatment marker for patients with esophageal cancer through decrease invasiveness of the disease and efficient response to neoadjuvant therapy.

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“…For example, miR-421 (targets: FXR, DPC4/SMAD4, ATM ), miR-503 (target: CCND1 ), miR-24-3p (targets: p27, p16 ), miR-29a (targets: PTEN, GSK3β, TET1 ) and miR-451 (targets: MIF, YWHAZ ) play a critical role in the proliferation, migration, invasion, and metastasis of BC. Additionally, miRNAs have a direct effect on ROS regulation, as will be seen in the next section ( 217 – 219 ).…”

Section: Interplay Between Mirnas and Ros In Breast Cancermentioning

confidence: 89%

A vicious circle in breast cancer: The interplay between inflammation, reactive oxygen species, and microRNAs

et al. 2022

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Breast cancer (BC) is the most common cancer in women worldwide. This highly heterogeneous disease is molecularly stratified into luminal A, luminal B, HER2, triple-negative/basal-like, and normal-like subtypes. An important aspect in BC progression is the activation of inflammatory processes. The activation of CD8+/Th1, NK, and M1 tumor associated macrophages (TAMs), leads to tumor destruction. In contrast, an anti-inflammatory response mediated by CD4+/Th2 and M2 TAMs will favor tumor progression. Inflammation also stimulates the production of inflammatory mediators like reactive oxygen species (ROS). In chronic inflammation, ROS activates oxidative stress and endothelial dysfunction. In cancer, ROS plays a dual role with anti-tumorigenic and pro-tumorigenic effects in cell signaling pathways that control proliferation, survival, apoptosis, and inflammation. MicroRNAs (miRNAs), which are known to be involved in BC progression and inflammation, can be regulated by ROS. At the same time, miRNAs regulate the expression of genes modulating oxidative stress. In this review, we will discuss the interplay between inflammation, ROS, and miRNAs as anticancer and tumor promoter molecules in BC. A clear understanding of the role of miRNAs in the regulation of ROS production and inflammation, may lead to new opportunities for therapy in BC.

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MicroRNAs Involved in Inflammatory Breast Cancer: Oncogene and Tumor Suppressors with Possible Targets

Cited by 8 publications

References 128 publications

MicroRNA-let-7 Targets HMGA2 to Regulate the Proliferation, Migration, and Invasion of Colon Cancer Cell HCT116

MicroRNA-let-7 Targets HMGA2 to Regulate the Proliferation, Migration, and Invasion of Colon Cancer Cell HCT116

EZH2 regulates oncomiR-200c and EMT markers in esophageal squamous cell carcinomas

A vicious circle in breast cancer: The interplay between inflammation, reactive oxygen species, and microRNAs

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