SOX2 oncogenes amplified and operate to activate AKT signaling in gastric cancer and predict immunotherapy responsiveness.

Abstract

INTRODUCTION:

Gastric cancer is the second leading cause of cancer mortality in the world. Whether the oncogene, amplified on chromosome 3q26, SOX2, a master transcriptional regulator of stemness, operate to drive strong growth phenotype in gastric cancer were unknown.

MATERIALS AND METHODS:

The gene expression changes of SOX2 in human gastric cancer tissues compared with non-cancerous tissues was detected using real-time quantitative reverse transcriptase-polymerase chain reaction (QRT-PCR) analysis and immunohistochemistry, which identified the gene overexpression of SOX2 in gastric cancer. Moreover, we discovered that SOX2 promoted cancer cell proliferation in vitro/vivo and SOX2 expression correlated with elevated AKT phosphorylation in gastric cancer, while the AKT phosphorylation was required for SOX2's oncogenic effects. Next, our data point to the usefulness of SOX2 overexpression, as a new predictive marker for responsiveness to trastuzumab.

CONCLUSION:

SOX2 is a commonly activated tumor promoter that activate AKT signaling in gastric cancer and a new predictive marker for targeted therapy.

• Authors: Yajun Tian, Xin Jia, Shengxiang Wang, Yongsheng Li, Peng Zhao, Da Cai, Zequan Zhou, Junmin Wang, Yi Luo, Maosheng Dong
• Journal: Journal of cancer research and clinical oncology (J Cancer Res Clin Oncol) Vol. 140 Issue 7 Pg. 1117-24 (Jul 2014) ISSN: 1432-1335 [Electronic] Germany
• PMID: 24752338 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Retracted Publication)

Chemical References

• SOX2 protein, human
• SOXB1 Transcription Factors
• Oncogene Protein v-akt

Topics

• Adult
• Aged
• Female
• Gene Amplification
• Gene Expression Regulation, Neoplastic
• Humans
• Immunotherapy
• Male
• Middle Aged
• Molecular Targeted Therapy
• Oncogene Protein v-akt (metabolism)
• Prognosis
• SOXB1 Transcription Factors (genetics, physiology)
• Signal Transduction (genetics)
• Stomach Neoplasms (genetics, therapy)
• Treatment Outcome