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2018 ; 9
(14
): 2451-2459
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Effect of FAM196B in human lung adenocarcinoma
#MMPMID30026842
Feng Y
; Tong X
; Zhang B
; Mao G
; Huang H
; Ma H
J Cancer
2018[]; 9
(14
): 2451-2459
PMID30026842
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Lung cancer is the leading cause of cancer-related mortality worldwide. The
present study focused on the function of family with sequence similarity 196
member B (FAM196B) in lung adenocarcinoma (LUAD). We analyzed lung carcinoma
patients' data from the Cancer Genome Atlas (TCGA), and verify the change of
FAM196B expression in 30 LUAD tissues and matched adjacent non-tumor tissues (> 5
cm) by tissue microarray. To investigate the role of FAM196B in LUAD, we used
lentivirus-mediated short hairpin RNA (shRNA) to knockdown FAM196B expression in
human LUAD cell line A549 and H1299 and assessed it by RT-qPCR and western blot.
Celigo Imaging Cytometry System, MTT assays and colony formation were conducted
to evaluate cell proliferation. Cell apoptosis were assayed by Annexin V
staining. We found that FAM196B was significantly upregulated (P=5.06E-06) in
LUAD compared with adjacent non-tumor tissues. Cell proliferation was inhibited
in FAM196B-silenced A549 and H1299 cells using Celigo Imaging Cytometry System,
MTT assays and colony formation assays. Apoptosis rate was significantly
increased in FAM196B-shRNA group than the control group. In conclusion, Knockdown
of FAM196B can inhibit cell proliferation, cell colony formation capacity, and
promote cell apoptosis in A549 and H1299 cell lines. FAM196B may be one novel
potential targets for treating patients with LUAD.
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