<p>miR-370-3p Alleviates Ulcerative Colitis-Related Colorectal Cancer in Mice Through Inhibiting the Inflammatory Response and Epithelial-Mesenchymal Transition</p>

Abstract

Introduction: Ulcerative colitis (UC) is a chronic and inflammatory bowel disease. UCassociated colorectal cancer (UC-CRC) is one of the most severe complications of long-standing UC. In the present study, we explored the effects of miR-370-3p on UC-CRC in vivo and investigated its underlying mechanisms in vivo and in vitro. Methods: Azoxymethane (AOM) and dextran sodium sulfate (DSS) were used to induce UC-CRC in C57BL/6 mice. AOM/DSS-induced mice were treated with 5×10 8 pfu miR-370-3p overexpressing-adenovirus via tail-vein injection every two weeks. Results: We found that miR-370-3p significantly improved the body weights and survival rates and inhibited the tumorigenesis of UC-CRC in AOM/DSS mice. Mechanically, miR-370-3p inhibited AOM/DSS-induced inflammatory response by decreasing tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6) through targeting toll-like receptor 4 (TLR4), as demonstrated by down-regulation of TLR4, cyclooxygenase-2 (COX-2), prostaglandin E2 (PGE2), and phosphorylated epidermal growth factor receptor (pEGFR). miR-370-3p decreased the expression of tumor-associated proteins, including p53, β-catenin, and ki67 in AOM/DSS-treated mice. Additionally, miR-370-3p remarkably inhibited epithelialmesenchymal transition (EMT) via increasing E-cadherin expression and reducing N-cadherin and Vimentin expression in vivo. Further studies showed that miR-370-3p repressed proliferation and EMT of colon cancer cells in vitro. Moreover, we proved that miR-370-3p decreased the expression of tumor-associated proteins and reversed EMT by regulating β-catenin in colon cancer cells. Conclusion: Taken together, miR-370-3p alleviated UC-CRC by inhibiting the inflammatory response and EMT in mice, which suggested miR-370-3p as a novel potential target for UC-CRC therapy.

<p>Circ_0058124 Aggravates the Progression of Papillary Thyroid Carcinoma by Activating LMO4 Expression via Targeting miR-370-3p</p>

“…MiR-370-3p was a well-recognized tumor suppressor in different types of cancers, including colorectal cancer, pituitary adenomas and glioma. [26][27][28] Likewise, the abundance of miR-370-3p was notably lower in thyroid cancer tissues relative to normal tissues, and miR-370-3p overexpression impaired viability and invasion of thyroid cancer cells. 15 Our study viewed that miR-370-3p expression was also declined in PTC tissues compared to normal tissues.…”

A Preliminary Study on the Pathogenesis of Colorectal Cancer by Constructing a Hsa-circRNA-0067835-miRNA-mRNA Regulatory Network

“…In addition, the hsa-circRNA-0067835/hsa-miR-197-3p, hsa-miR-370-3p, and hsa-miR-377-5p signal axes were initially determined. One study has shown that hsa-miR -370-3p reduces ulcerative colitis-related CRC by inhibiting inflammation and epithelial-mesenchymal transition; 21 Hsa-circ-0002024 inhibits bladder cancer cell proliferation, migration and invasion by sponging miR-197-3p. 22 The above results suggest that both hsa-miR-197-3p and hsa-miR-370-3p are related to cancer.…”

MicroRNAs in Epithelial–Mesenchymal Transition Process of Cancer: Potential Targets for Chemotherapy

“…MiR-370-3p played a key role in repressing CRC proliferation and EMT in vitro. The underlying mechanism proved that miR-370-3p could reduce tumor-related inflammatory factors, such as TNF- , IL-1 β, and IL-6, thereby inhibiting proteins such as P53, β-catenin, and ki67, which are closely related to tumor growth [ 67 ]. MiR-873-5p overexpression dramatically inhibited CRC cell proliferation and EMT.…”