Abstract
As an important global medical problem, hepatocellular carcinoma (HCC) has been recognized as the most frequent primary liver cancer and a leading cause of death among patients with cirrhosis. Surveillance of HCC using serum markers aims to reduce the disease-related mortality of HCC. MUC16 (mucin 16, also known as carbohydrate antigen 125, CA125) has been predicted as a tumor biomarker for many cancer types. Based on the high frequency mutation rate in a database from the Cancer Genome Atlas (TCGA), we investigated the effects of MUC16 knockdown and the regulatory profile of MUC16 in HepG2 and Huh7 cell lines. Knockdown of MUC16 was conducted via siRNA transfection, and the proliferation of cells was not affected by CCK8 assay results. Moreover, decreasing the expression of MUC16 enhanced the migration and invasion of cells, as shown by wound healing and transwell assays. Furthermore, RNA-seq was used to investigate the effect of MUC16 knockdown on the gene expression profile of HepG2 and Huh7 cells. Our study demonstrated the significant role of MUC16 in the inhibition of the migration and invasion of HepG2 and Huh7 cells.
Highlights
Hepatocellular carcinoma (HCC) accounts for more than 80% of primary liver cancers and ranks as the third leading cause of cancer-related mortality worldwide [1, 2]
Our results demonstrated that MUC16 knockdown enhanced the wound healing, migration and invasion abilities of hepatoma cancer cells but did not significantly affect cell proliferation
It is considered that serum CA125 was generated from HCC tissue, we examined oncogene mutations in the Cancer Genome Atlas (TCGA)’s liver cancer project
Summary
Hepatocellular carcinoma (HCC) accounts for more than 80% of primary liver cancers and ranks as the third leading cause of cancer-related mortality worldwide [1, 2]. In China, owing to the high rate of chronic hepatitis B virus (HBV) infection, HCC accounts for nearly 55% of all global HCC cases [3]. The prognosis and survival of HCC patients remain disappointing because of the high rate of recurrence and metastasis [4, 5]. Many molecular biomarkers involved in HCC have been identified, the mechanism behinds its development remains unclear. In 1981, a high molecular weight protein expressed on the surface of ovarian cancer cells was recognized by a monoclonal antibody selectively targeting MUC16, and it was subsequently found There have been continuous efforts to discover HCC-associated autoantibody biomarkers for use as early diagnostic biomarkers, and several tumor-associated autoantibodies were recently suggested as early predictors of HCC before diagnosis [6, 7].
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