Tropomyosin3 overexpression and a potential link to epithelial-mesenchymal transition in human hepatocellular carcinoma
2010

The Role of Tropomyosin3 in Liver Cancer

Sample size: 2 publication Evidence: high

Author Information

Author(s): Choi Hye-Sun, Yim Seon-Hee, Xu Hai-Dong, Jung Seung-Hyun, Shin Seung-Hun, Hu Hae-Jin, Jung Chan-Kwon, Choi Jong Young, Chung Yeun-Jun

Primary Institution: The Catholic University of Korea

Hypothesis

Overexpression of TPM3 activates Snail mediated EMT, which represses E-cadherin expression and confers migration or invasion potentials to HCC cells during hepatocarcinogenesis.

Conclusion

TPM3 knockdown significantly reduces the migration and invasion of hepatocellular carcinoma cells.

Supporting Evidence

  • Silencing TPM3 resulted in significant suppression of migration and invasion capacities in both HCC cell lines.
  • E-cadherin expression was significantly upregulated and Snail downregulated after TPM3 knockdown.
  • TPM3 knockdown inhibited colony formation and anchorage independent growth of HCC cells.

Takeaway

When a protein called TPM3 is turned off in liver cancer cells, they have a harder time moving and spreading.

Methodology

TPM3 was silenced using siRNA in two HCC cell lines, and effects on migration, invasion, and growth were assessed.

Limitations

The study did not examine the direct binding of TPM3 to Snail and the biological consequences of TPM3 overexpression were not fully established.

Statistical Information

P-Value

<0.0001

Confidence Interval

95% CI 0.03-0.06

Statistical Significance

p<0.0001

Digital Object Identifier (DOI)

10.1186/1471-2407-10-122

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