miR‐32 promotes esophageal squamous cell carcinoma metastasis by targeting CXXC5

MicroRNA‐32 (miR‐32) functioned as a tumor oncogene in some cancer, which control genes involved in important biological and pathological functions and facilitate the tumor growth and metastasis. However, the role of miR‐32 modulates esophageal squamous cell carcinoma (ESCC) malignant transformation has not been clarified. Here, we focused on the function and the underlying molecular mechanism of miR‐32 in ESCC. Results discovered a significant increased expression of miR‐32 in ESCC tissues and cells. Downregulation of miR‐32 inhibited the migration, invasion, adhesion of ESCC cell lines (EC9706 and KYSE450), and the levels of EMT protein in vitro. In vivo, miR‐32 inhibitors decrease tumor size, tumor weight, and the number of metastatic nodules. Hematoxylin and eosin (H&E) results revealed that inhibition of miR‐32 attenuate lung metastasis. Immunohistochemistry and immunofluorescence assay showed increased level of E‐cadherin and decreased level of N‐cadherin and Vimentin with treatment of miR‐32 inhibitors. Furthermore, miR‐32 targeted the 3′‐untranslated region (3′‐UTR) of CXXC5, and inhibited the level of mRNA and protein of CXXC5. There is a negative correlation between the expressions of CXXC5 and miR‐32. Then, after EC9706 and KYSE450 cells cotransfected with si‐CXXC5 and miR‐32 inhibitors, the ability of cell migration, invasion, and adhesion was significantly reduced. In addition, the protein expression of EMT and TGF‐β signaling was also depressed. Collectively, these data supply an insight into the positive role of miR‐32 in ESCC progression and metastasis, and its biological effects may attribute the inhibition of TGF‐β signaling mediated by CXXC5. MicroRNA‐32 (miR‐32) could promote esophageal squamous cell carcinoma (ESCC) migration, invasion, and adhesion via target CXXC5. miR‐32 might be a key oncogene of ECSS metastasis through inhibiting CXXC5‐mediated TGF‐β pathway