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PIN1 expression contributes to hepatic carcinogenesis.

R W Pang¹, T K Lee, K Man

¹Department of Medicine, University of Hong Kong, Queen Mary Hospital, Pokfulam Road, Hong Kong.

The Journal of Pathology

|July 15, 2006

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Prolyl isomerase PIN1 overexpression drives hepatocellular carcinoma (HCC) development by increasing beta-catenin and cyclin D1. Suppressing PIN1 inhibits HCC cell growth and tumorigenicity, implicating PIN1 in liver cancer progression.

Area of Science:

Oncology
Molecular Biology
Hepatology

Background:

Prolyl isomerase PIN1 (Peptidyl-prolyl cis-trans isomerase NIMA-interacting 1) is overexpressed in over 50% of hepatocellular carcinomas (HCCs).
PIN1's role in hepatocarcinogenesis remains to be fully elucidated.

Purpose of the Study:

To investigate the oncogenic potential of PIN1 in hepatocellular carcinoma.
To determine the effect of PIN1 modulation on HCC cell behavior and tumorigenicity.

Main Methods:

Overexpression of PIN1 in non-transformed human liver MIHA cells.
Suppression of PIN1 using RNA interference (siRNA) in the HCC cell line PLC/PRF/5.
Assessment of beta-catenin and cyclin D1 levels, cell proliferation, cell cycle progression, soft agar colony formation, and tumorigenicity in nude mice.

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Main Results:

PIN1 overexpression in MIHA cells led to increased beta-catenin and cyclin D1, promoting anchorage-independent growth and tumorigenicity.
PIN1 suppression in PLC/PRF/5 cells decreased beta-catenin and cyclin D1 levels, reducing cell proliferation, colony formation, and cell cycle progression.
siRNA-mediated PIN1 knockdown abrogated soft agar colony formation and tumorigenicity in nude mice.

Conclusions:

PIN1 overexpression is a critical factor in hepatic carcinogenesis.
PIN1 plays a significant role in promoting HCC development and progression.
Targeting PIN1 may represent a therapeutic strategy for hepatocellular carcinoma.