Serine/Arginine Repetitive Matrix 2 Antisense RNA 1 Negatively Regulates miR-370-3p and Promotes Hyperplasia, Migration, and Aggression of the Colon Cancer Cell Line

The purpose of this study is to explore the effect and possible machine-processing of the long non-coding RNA (lncRNA) SRRM2-AS1 in the development and pathogenesis of colorectal cancer. LncRNA plays an important role in tumorigenesis and development. LncRNA can regulate gene transcription and translation, cell proliferation, differentiation and apoptosis by affecting gene expression pathways of various coding proteins. SRRM2-AS1 is a kind of lncRNA. Studies have confirmed that the expression of SRRM2-AS1 is increased in colon adenocarcinoma tissues of colon cancer patients and is closely related to the prognosis of patients. However, the influence and molecular mechanism of SRRM2-AS1 on the malignant biological behavior of colon cancer cells are no yet clear. SRRM2-AS1 may interact with miR-370-3p. Studies have confirmed that overexpression of miR-370-3p can inhibit the proliferation and epithelial-mesenchymal transition of colon cancer cells in vitro. However, it is not yet clear whether SRRM2-AS1 can target miR-370-3p to affect the occurrence and development of tumors. In this study, RT-qPCR was employed to detect levels of SRRM2-AS1 and miRNA-370-3p in carcinoma tissues and corresponding paracarcinoma tissues from 41 patients with colon cancer. SW1116 colon cancer cells were cultured in vitro and separated into 4 groups: (1) si-NC group, (2) si-SRRM2-AS1 group, (3) si-SRRM2-AS1+anti-miRNA-NC group, and (4) si-SRRM2-AS1+anti-miRNA-370-3p group. The CCK-8 assay and colony formation experiment was employed to gauge cell proliferation. The scratch test was used to detect cell migration while the transwell assay was used to detect cell invasion. Finally, Western blot analysis was employed to detect levels of Ki67, E-cadherin, and N-cadherin proteins in colorectal cancer cells. The dual-luciferase reporter gene experiment verified that SRRM2-AS1 regulates miRNA-370-3p. The study found that compared to paracarcinoma tissue, levels of SRRM2-AS1 in colon cancer tissues was increased (P < 0.05). Compared to the si-NC group, the SW1116 cell OD value, number of colonies formed, scratch healing rate, number of invasive cells, and expression levels of Ki67 and N-cadherin protein in the si-SRRM2-AS1 group were all decreased (P < 0.05). However, E-cadherin protein levels were elevated (P < 0.05). SRRM2-AS1 negatively regulates levels of miRNA-370-3p in SW1116 cells. Compared to the si-SRRM2-AS1+anti-miRNA-NC group, SW1116 cell OD value, number of colonies formed, scratch healing rate, number of invasive cells, and Ki67 and N-cadherin protein levels were increased (P < 0.05) in the si-SRRM2-AS1+anti-miRNA-370-3p group. Conversely, E-cadherin protein levels were decreased (P < 0.05). These findings indicate that SRRM2-AS1 is predominately expressed in cancerous colon tissues. Attenuating expression of SRRM2-AS1 may curb the hyperplasia of colon carcinoma cell line SW1116 and promote cell apoptosis by regulating miRNA-370-3p expression.