
MIR-147B REGULATED PROLIFERATION
AND APOPTOSIS OF GASTRIC CANCER CELLS
BY TARGETING CPEB2 VIA THE PTEN PATHWAY Tao K.1,2, Dong J-H.2, Wang D.1, Li F.2†#, Zhang Z-T.#1* *Corresponding Author: Zhong-Tao Zhang, MD, Email: sxzhangzhongtao@sina.com, ORCID ID: 0000-0002-1184-2591
#: Zhong-Tao Zhang and Feng Li contributed equally to the article
†: Co-corresponding author: Feng Li, Email: sxlifengwobuxin@sina.com, ORCID: 0000-0002-7322-422X page: 10
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INTRODUCTION
Over the last four decades, the world has experienced
rapid demographic and epidemiological transitions. Rapid
industrialization, urbanization, aging, and changes in
lifestyle have led to a shift in the burden of the disease
spectrum from infectious diseases to non‐communicable
diseases. China has been an important contributor to the
global cancer burden because of its large population.
Among the cancer related deaths, Gastric cancer (GC)
ranked fifth and was responsible for a significant mortality
rates across the globe1. Particularly in China, the survivability
of patients in after 5years is only 30 % after radical
resection2, 3. Therefore, it is urgent to study the mechanism
of GC occurrence and development4.
MicroRNAs (miRNAs) are a family of small noncoding
RNAs of 20–22 nucleotides that regulate a wide
array of biological processes including carcinogenesis.
Under normal physiological conditions, miRNAs function
in feedback mechanisms by safeguarding key biological
processes including cell proliferation, differentiation
and apoptosis5. However, in cancer cells, miRNAs have
been found to be heavily dysregulated and are considered
to play a pivotal role in the progression of a variety of
tumors. It can reverse mediate about 30-40% of human
genes by binding to the complementary 3 ‘- non expression
region (3’ - UTR)6,7. Recent studies have shown that
miR-147b is related to some cancers 8, which may be the
tumor suppressor gene or oncogene. Over-expression of
the miR-147b inhibitor or SOX15 can be seen through the Wnt/β-Catenin signal transduction pathway, delaying the
growth of cancer cells in vivo. The role of miR-147b in
GC is not clear; therefore, we have conducted the present
study to elucidate its probable mechanism in GC.
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