Sorcin induces gastric cancer cell migration and invasion contributing to STAT3 activation
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Huan Tuo1,*, Feng Shu1,*, Sha She1, Min Yang1, Xiao Qin Zou1, Juan Huang1, Huai Dong Hu1,2, Peng Hu1,2,3, Hong Ren1,2,3, Shi Fang Peng4,5 and Yi Xuan Yang1,2,3
1Department of Infectious Diseases, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, China
2Institute for Viral Hepatitis of Chongqing Medical University, Chongqing 400016, China
3Key Laboratory of Molecular Biology for Infectious Diseases, Ministry of Education, Chongqing Medical University, Chongqing 400016, China
4Department of Infectious Diseases, Xiangya Hospital, Central South University, Hunan 410008, China
5Department of Health Management Center, Xiangya Hospital, Central South University, Hunan 410008, China
*These authors have contributed equally to this work
Yi Xuan Yang, email: [email protected]
Shi Fang Peng, email: [email protected]
Keywords: gastric cancer (GC); sorcin; migration; invasion; iTRAQ
Received: July 08, 2017 Accepted: September 21, 2017 Published: October 31, 2017
Gastric cancer (GC) is a globally occurring malignancy that is characterized by a high mortality rate due to a high tendency to metastasize and poor prognoses. Sorcin, as known as SRI, a soluble resistance-related calcium-binding protein, plays a significant role in multidrug resistance. Sorcin is related to the migration and invasion of cancer cells. However, the mechanism remains unclear. Here, we used immunohistochemistry to confirm that the expression of sorcin in cancer tissues is higher than that in the adjacent normal tissues. The wound healing and transwell results indicate that sorcin can induce migration and invasion of GC cells. To explore the role of sorcin in GC metastasis, isobaric tags for relative and absolutely quantitation (iTRAQ) were used to examine cells with and without sorcin knockdown to identify the differentially expressed proteins (DEPs). The results were evaluated via RT-PCR and western blot to confirm the ITRAQ data. Inhibition of sorcin expression can down- regulate the expression of CTSZ, MMP2, MMP9 and p-STAT3 followed by suppression of tumor growth and metastasis. Together, we concluded that sorcin has a oncogenic activity via inducing tumor growth and metastasis, leading to development of therapeutic treatments for GC.
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