Down-regulation of tensin2 enhances tumorigenicity and is associated with a variety of cancers

Shiao Ya Hong, Yi Ping Shih, Peng Sun, Wang Ju Hsieh, Wen Chang Lin, Su Hao Lo

Research output: Contribution to journalArticle

6 Scopus citations

Abstract

Tensin family members, including tensin2 (TNS2), are present as major components of the focal adhesions. The N-terminal end of TNS2 contains a C1 region (protein kinase C conserved region 1) that is not found in other tensin members. Three isoforms of TNS2 have been identified with previous reports describing the shortest V3 isoform as lacking the C1 region. Although TNS2 is known to regulate cell proliferation and migration, its role in tumorigenicity is controversial. By gain-offunction overexpression approaches, results supporting either promotion or reduction of cancer cell tumorigenicity were reported. Here we report that the complete V3 isoform also contains the C1 region and describe the expression patterns of the three human TNS2 isoforms. By loss-of-function approaches, we show that silencing of TNS2 up-regulates the activities of Akt, Mek, and IRS1, and increases tumorigenicities in A549 and Hela cells. Using public database analyses we found that TNS2 is downregulated in head and neck, esophageal, breast, lung, liver, and colon cancer. In addition, patients with low TNS2 expression showed poor relapse-free survival rates for breast and lung cancers. These results strongly suggest a role of tensin2 in suppressing cell transformation and reduction of tumorigenicity.

Original languageEnglish (US)
Pages (from-to)38143-38153
Number of pages11
JournalOncotarget
Volume7
Issue number25
DOIs
StatePublished - 2016

Keywords

  • Focal adhesion
  • IRS1
  • Mek
  • Tensin
  • Tumorigenesis

ASJC Scopus subject areas

  • Oncology

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