MiR-142-5p Acts as a Significant Regulator Through Promoting Proliferation, Invasion, and Migration in Breast Cancer Modulated by Targeting SORBS1

Abstract

Background: Numerous researches have demonstrated that miR-142-5p plays significant roles in several cancers, although the functional characteristic of miR-142-5p in breast cancer has not been determined. This study is designed to explore the biological significance of miR-142-5p in breast cancer clinical implication and mechanism of action. Methods: The differential expression patterns of miR-142-5p and Sorbin and SH3 domain-containing protein 1 and correlations between them and clinical significances were analyzed based on data from database. The expression levels of miR-142-5p in breast cancer cells were detected using quantitative real-time polymerase chain reaction. Cell counting kit-8, transwell, and wound healing assays were used to explore the potential functions of miR-142-5p in breast cancer cells. In addition, bioinformatics prediction analysis and luciferase reporter assay were utilized to predict and identify the potential target gene of miR-142-5p. A rescue experiment was conducted by transfecting miR-142-5p inhibitors and si-Sorbin and SH3 domain-containing protein 1 into cells to explore miR-142-5p/Sorbin and SH3 domain-containing protein 1 pairs on breast cancer cells behaviors. Results: The analysis results showed that miR-142-5p was highly expressed in patients with breast cancer, while Sorbin and SH3 domain-containing protein 1 presented a trend of low expression. The clinical significances analysis suggested that the overexpression of miR-142-5p is closely correlated with metastasis, while low expression of Sorbin and SH3 domain-containing protein 1 is correlated with clinicopathological characteristics and poor overall survival in patients with breast cancer. In vitro exploration, the expression of miR-142-5p was upregulated in breast cancer cells and inhibition of miR-142-5p expression significantly reduced the proliferation, invasion, and migration of breast cancer cells. Through rescue experiments, breast cancer cells proliferation, invasion, and migration reduction induced by silencing of miR-142-5p were reversed via knockdown Sorbin and SH3 domaincontaining protein 1. Conclusion: Our findings insinuate that miR-142-5p functions as a positive regulator of promoting breast cancer cells biological behaviors and clinical metastasis, possibly regulated by targeting Sorbin and SH3 domain-containing protein 1, thus providing valuable information in the development of preventive or even therapeutic strategies for utilizing miR-142-5p as a promising target.

Circ_0001944 Contributes to Glycolysis and Tumor Growth by Upregulating NFAT5 Through Acting as a Decoy for miR-142-5p in Non-Small Cell Lung Cancer

“…Previous studies had reported that miR-142-5p repressed the advancement of gastric cancer, breast cancer, and cervical cancer by, respectively, targeting CYR61, SORBS1, and PIK3AP1. [22][23][24] However, miR-142-5p played a carcinogenic role in renal cell cancer and colorectal cancer. 25,26 In addition, miR-142-5p exerted a tumorrepressive role in lung cancer.…”

Screening differentially expressed genes between endometriosis and ovarian cancer to find new biomarkers for endometriosis

“…By analysing the GO functions of these 11 DEGs, we found that ITGA7 , ITGBL1 and SORBS1 were mainly involved in cell adhesion ( Table 3 ). We observed that ITGA7 had a direct interaction with ITGBL1 in PPI network ( Figure 3 ), which suggested that they might be coexpressed, and all three genes were upregulated DEGs that regulated cell proliferation, invasion and migration in cancers [ 47–51 ]. It is of great significance to analyse their survival in obstetrics- and gynaecology-related tumours ( Figure 6 ).…”

“…Moreover, it promoted epithelial-to-mesenchymal transition (EMT) of colorectal cancer (CRC) cells [ 55 ] and had the same characteristics in ovarian cancer [ 51 ] and prostate cancer [ 50 ]. SORBS1 overexpression promoted CRC growth and migration via inhibition of AHNAK expression [ 56 ], while SORBS1 was downregulated in breast cancer and led to poor prognosis [ 47 ]. Silencing of SORBS1 promoted the EMT process and attenuated chemical drug sensitivity, and it is a potential inhibitor of metastasis in cancer [ 57 ].…”

Study on <em>CCDC69</em> interfering with the prognosis of patients with breast cancer through PPAR signal pathway

“…29 Yu et al demonstrated that miR-142-5p promotes proliferation, invasion, and migration of breast cancer by targeting SORBS1. 45 Song et al revealed that SORBS1 silencing increases the migration and invasion of breast cancer cells by activating JNK/cJun and promotes EMT. The chemosensitivity was reduced by inhibiting p53.…”