PTPRG suppresses tumor growth and invasion via inhibition of Akt signaling in nasopharyngeal carcinoma

Arthur Kwok Leung Cheung, Joseph Chok Yan Ip, Adrian Chi Hang Chu, Yue Cheng, Merrin Man Long Leong, Josephine Mun Yee Ko, Wai Ho Shuen, Hong Lok Lung, Maria Li Lung*

*Corresponding author for this work

Research output: Contribution to journalJournal articlepeer-review

36 Citations (Scopus)

Abstract

Protein Tyrosine Phosphatase, Receptor Type G (PTPRG) was identified as a candidate tumor suppressor gene in nasopharyngeal carcinoma (NPC). PTPRG induces significant in vivo tumor suppression in NPC. We identified EGFR as a PTPRG potential interacting partner and examined this interaction. Dephosphorylation of EGFR at EGFR-Y1068 and -Y1086 sites inactivated the PI3K/Akt signaling cascade and subsequent down-regulation of downstream pro-angiogenic and -invasive proteins (VEGF, IL6, and IL8) and suppressed tumor cell proliferation, angiogenesis, and invasion. The effect of Akt inhibition in NPC cells was further validated by Akt knockdown experiments in the PTPRG-down-regulated NPC cell lines. Our results suggested that inhibition of Akt in NPC cells induces tumor suppression at both the in vitro and in vivo levels, and also importantly, in vivo metastasis. In conclusion, we confirmed the vital role of PTPRG in inhibiting Akt signaling with the resultant suppression of in vivo tumorigenesis and metastasis.

Original languageEnglish
Pages (from-to)13434-13447
Number of pages14
JournalOncotarget
Volume6
Issue number15
DOIs
Publication statusPublished - 30 May 2015
Externally publishedYes

Scopus Subject Areas

  • Oncology

User-Defined Keywords

  • Akt
  • EGFR
  • Nasopharyngeal carcinoma
  • PTPRG
  • Tumor suppressor

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