4.4 Article

Tazarotene-induced gene 1 interacts with Polo-like kinase 2 and inhibits cell proliferation in HCT116 colorectal cancer cells

Journal

CELL BIOLOGY INTERNATIONAL
Volume 45, Issue 11, Pages 2347-2356

Publisher

WILEY
DOI: 10.1002/cbin.11681

Keywords

cell proliferation; cyclin E1; Fbxw7; Polo-like kinases; tazarotene-induced gene 1

Categories

Funding

  1. Core Laboratory of the Buddhist Tzu Chi General Hospital
  2. Taipei Tzu Chi Hospital through Buddhist Tzu Chi Medical Foundation, Taipei, Taiwan [TCRD-TPE-110-13, TCRD-TPE110-27]

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The study revealed that TIG1 regulates the tumorigenesis of CRC by modulating the activity of PLK2. The expression of PLK2 in CRC cells is associated with low levels of Fbxw7 protein and increased expression of cyclin E1. The findings suggest a potential mechanism for CRC development and progression involving the interaction between TIG1 and PLK2.
Tazarotene-induced gene 1 (TIG1) is considered to be a tumor suppressor gene that is highly expressed in normal or well-differentiated colon tissues, while downregulation of TIG1 expression occurs in poorly differentiated colorectal cancer (CRC) tissues. However, it is still unclear how TIG1 regulates the tumorigenesis of CRC. Polo-like kinases (Plks) are believed to play an important role in regulating the cell cycle. The performance of PLK2 in CRC is negatively correlated with the differentiation status of CRC tissues. Here, we found that PLK2 can induce the growth of CRC cells and that TIG1 can prevent PLK2 from promoting the proliferation of CRC cells. We also found that the expression of PLK2 in CRC cells was associated with low levels of Fbxw7 protein and increased expression of cyclin E1. When TIG1 was coexpressed with PLK2, the changes in Fbxw7/cyclin E1 levels induced by PLK2 were reversed. In contrast, silencing TIG1 promoted the proliferation of CRC, and when PLK2 was also silenced, the proliferation of CRC cells induced by TIG1 silencing was significantly inhibited. The above research results suggest that TIG1 can regulate the tumorigenesis of CRC by regulating the activity of PLK2.

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