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Knockdown of TMEM16A suppressed MAPK and inhibited cell proliferation and migration in hepatocellular carcinoma
Liang Deng1, Jihong Yang2, Hongwu Chen3
1Department of Hepatobiliary Surgery, The Eastern Hospital of the First Affiliated Hospital of Sun Yat-sen University, Guangzhou, People's Republic of China.
Abstract:
TMEM16A plays an important role in cell proliferation in various cancers. However, less was known about the expression and role of TMEM16A in hepatocellular carcinoma. We screened the expression of TMEM16A in patients' hepatocellular carcinoma tissues, and also analyzed the biological function of hepatocellular carcinoma cells by knockdown of TMEM16A, as well as the expression of MAPK signaling proteins, including p38, p-p38, ERK1/2, p-ERK1/2, JNK, and p-JNK, and cell cycle regulatory protein cyclin D1 in TMEM16A siRNA-transfected SMMC-7721 cells by Western blot. Our results showed that TMEM16A was overexpressed in hepatocellular carcinoma tissues. Inhibition of TMEM16A suppressed the cell proliferation, migration, and invasion, and cell cycle progression but did not influence the cell apoptosis. TMEM16A siRNA-suppressed cancer cell proliferation and tumor growth were accompanied by a reduction of p38 and ERK1/2 activation and cyclin D1 induction, and were not influenced by other tested MAPK signaling proteins. In addition, inhibition of TMEM16A suppressed tumorigenicity in vivo. TMEM16A is overexpressed in hepatocellular carcinoma, and that inhibition of TMEM16A suppressed MAPK and growth of hepatocellular carcinoma. TMEM16A could be a potentially novel therapeutic target for human cancers, including hepatocellular carcinoma.
Insights
Transmembrane protein 16A (TMEM16A) is overexpressed in hepatocellular carcinoma. Inhibiting TMEM16A suppressed cancer growth by reducing MAPK signaling, suggesting it as a potential therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Transmembrane protein 16A (TMEM16A) is implicated in cell proliferation across various cancers.
- The specific role and expression of TMEM16A in hepatocellular carcinoma (HCC) remain largely uncharacterized.
Purpose of the Study:
- To investigate the expression and functional role of TMEM16A in hepatocellular carcinoma.
- To explore the impact of TMEM16A inhibition on HCC cell behavior and associated signaling pathways.
Main Methods:
- Screening TMEM16A expression in HCC patient tissues.
- Utilizing TMEM16A siRNA to knockdown expression in SMMC-7721 HCC cells.
- Analyzing cell proliferation, migration, invasion, apoptosis, cell cycle progression, and MAPK signaling proteins (p38, ERK1/2, JNK) via Western blot.
- Assessing tumorigenicity in vivo.
Main Results:
- TMEM16A was found to be significantly overexpressed in HCC tissues.
- Inhibition of TMEM16A suppressed HCC cell proliferation, migration, invasion, and cell cycle progression, without affecting apoptosis.
- TMEM16A knockdown led to reduced activation of p38 and ERK1/2 pathways and decreased cyclin D1 levels.
- Inhibition of TMEM16A also suppressed tumor growth in vivo.
Conclusions:
- TMEM16A overexpression is a feature of hepatocellular carcinoma.
- TMEM16A inhibition effectively suppresses HCC progression by modulating MAPK signaling and cell cycle.
- TMEM16A presents a promising novel therapeutic target for hepatocellular carcinoma and potentially other human cancers.
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