Open AccessLnc RNA ‐ SNHG 15 enhances cell proliferation in colorectal cancer by inhibiting miR‐338‐3p
Author(s) -
Li Min,
Bian Zehua,
Jin Guoying,
Zhang Jia,
Yao Surui,
Feng Yuyang,
Wang Xue,
Yin Yuan,
Fei Bojian,
You Qingjun,
Huang Zhaohui
Publication year - 2019
Publication title -
cancer medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 53
ISSN - 2045-7634
DOI - 10.1002/cam4.2105
Subject(s) - cell growth , apoptosis , in vivo , biology , rna , cancer research , colorectal cancer , microbiology and biotechnology , flow cytometry , long non coding rna , cancer , gene , biochemistry , genetics
The incidence and death rate of colorectal cancer ( CRC ) is very high, which brings great need to understand the early molecular events of CRC . These studies demonstrate that long noncoding RNA (lnc RNA ) plays an important role in the occurrence and development of human cancer. Small nucleolar RNA host gene 15 ( SNHG 15) was recently identified as a cancer‐related lnc RNA . In this study, we aimed to evaluate the function and mechanism of SNHG 15 in CRC . The expression of SNHG 15 was detected by quantitative RT ‐ PCR ( qRT ‐ PCR ) in CRC tissues and matched noncancerous tissues ( NCT s). CCK ‐8 assay, colony formation assay, flow cytometric analysis, and nude mouse xenograft mode were used to examine the tumor‐promoting function of SNHG 15 in vitro and in vivo. The binding relationship between SNHG 15, miR‐338‐3p and the target genes of miR‐338‐3p were screened and identified by databases, qRT ‐ PCR , dual luciferase reporter assay and western blot. Our results showed that SNHG 15 was up‐regulated in CRC tissues compared with paired NCT s ( P < 0.0001). High level of SNHG 15 expression predicted poor prognosis of CRC ( P = 0.0051). SNHG 15 overexpression could promote cell proliferation and inhibit cell apoptosis. Animal experiments showed that up‐regulation of SNHG 15 promoted tumor growth in vivo. The results of mechanism experiments showed that SNHG 15 could bind to miR‐338‐3p and block its inhibition on the expression and activity of FOS or RAB 14. In conclusion SNHG 15 promotes cell proliferation through SNHG 15/miR‐338‐3p/ FOS ‐ RAB 14 axis in CRC.