PTEN loss induces epithelial - Mesenchymal transition in human colon cancer cells

Kanika Bowen-Jallow, Hung Q. Doan, Binhua P. Zhou, Qingding Wang, Yuning Zhou, Piotr G. Rychahou, B. Mark Evers

Research output: Contribution to journalArticle

62 Citations (Scopus)

Abstract

Background: The epithelial-mesenchymal transition is a critical early event in the invasion and metastasis of many types of cancer, including colorectal cancer (CRC). Chronic inflammation is an inducer of several cancer types and inflammatory cytokines have been implicated in tumor invasion. Materials and Methods: Human colon cancer cell lines HCT116 and SW480 were transfected with phosphatase and tensin homolog deleted on chromosome 10 (PTEN) siRNA or non-targeting control (NTC). Invasiveness was measured using a modified Boyden chamber assay and migration was assessed using a scratch assay. Results: PTEN knockdown increased the invasion and migration of CRC cells and the addition of medium containing tumor necrosis factor-α (TNF-α) further enhanced the migration and invasion. PTEN knockdown resulted in nuclear β-catenin accumulation and increased expression of downstream proteins c-Myc and cyclin D1. Conclusion: Our study supports the findings of clinical studies identifying an association of PTEN loss with late stage cancer. Cellular factors secreted from the surrounding tumor milieu likely act in concert with genetic changes in the tumor cells and contribute to enhanced tumor invasion.

Original languageEnglish (US)
Pages (from-to)4439-4449
Number of pages11
JournalAnticancer Research
Volume29
Issue number11
StatePublished - Nov 2009

Fingerprint

Epithelial-Mesenchymal Transition
Colonic Neoplasms
Neoplasms
Colorectal Neoplasms
Proto-Oncogene Proteins c-myc
Catenins
Chromosomes, Human, Pair 10
Cyclin D1
Phosphoric Monoester Hydrolases
Small Interfering RNA
Tumor Necrosis Factor-alpha
Cytokines
Neoplasm Metastasis
Inflammation
Cell Line

Keywords

  • EMT
  • Invasion
  • Migration
  • PTEN
  • TNF-α

ASJC Scopus subject areas

  • Cancer Research
  • Oncology

Cite this

Bowen-Jallow, K., Doan, H. Q., Zhou, B. P., Wang, Q., Zhou, Y., Rychahou, P. G., & Evers, B. M. (2009). PTEN loss induces epithelial - Mesenchymal transition in human colon cancer cells. Anticancer Research, 29(11), 4439-4449.

PTEN loss induces epithelial - Mesenchymal transition in human colon cancer cells. / Bowen-Jallow, Kanika; Doan, Hung Q.; Zhou, Binhua P.; Wang, Qingding; Zhou, Yuning; Rychahou, Piotr G.; Evers, B. Mark.

In: Anticancer Research, Vol. 29, No. 11, 11.2009, p. 4439-4449.

Research output: Contribution to journalArticle

Bowen-Jallow, K, Doan, HQ, Zhou, BP, Wang, Q, Zhou, Y, Rychahou, PG & Evers, BM 2009, 'PTEN loss induces epithelial - Mesenchymal transition in human colon cancer cells', Anticancer Research, vol. 29, no. 11, pp. 4439-4449.
Bowen-Jallow K, Doan HQ, Zhou BP, Wang Q, Zhou Y, Rychahou PG et al. PTEN loss induces epithelial - Mesenchymal transition in human colon cancer cells. Anticancer Research. 2009 Nov;29(11):4439-4449.
Bowen-Jallow, Kanika ; Doan, Hung Q. ; Zhou, Binhua P. ; Wang, Qingding ; Zhou, Yuning ; Rychahou, Piotr G. ; Evers, B. Mark. / PTEN loss induces epithelial - Mesenchymal transition in human colon cancer cells. In: Anticancer Research. 2009 ; Vol. 29, No. 11. pp. 4439-4449.
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AB - Background: The epithelial-mesenchymal transition is a critical early event in the invasion and metastasis of many types of cancer, including colorectal cancer (CRC). Chronic inflammation is an inducer of several cancer types and inflammatory cytokines have been implicated in tumor invasion. Materials and Methods: Human colon cancer cell lines HCT116 and SW480 were transfected with phosphatase and tensin homolog deleted on chromosome 10 (PTEN) siRNA or non-targeting control (NTC). Invasiveness was measured using a modified Boyden chamber assay and migration was assessed using a scratch assay. Results: PTEN knockdown increased the invasion and migration of CRC cells and the addition of medium containing tumor necrosis factor-α (TNF-α) further enhanced the migration and invasion. PTEN knockdown resulted in nuclear β-catenin accumulation and increased expression of downstream proteins c-Myc and cyclin D1. Conclusion: Our study supports the findings of clinical studies identifying an association of PTEN loss with late stage cancer. Cellular factors secreted from the surrounding tumor milieu likely act in concert with genetic changes in the tumor cells and contribute to enhanced tumor invasion.

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