FAM107B is regulated by S100A4 and mediates the effect of S100A4 on the proliferation and migration of MGC803 gastric cancer cells

Abstract

FAM107B expression was decreased in stomach cancer and many other kinds of cancer. The forced expression of FAM107B in HeLa cells diminished proliferation in response to growth factors, suggesting that FAM107B might play important roles in many types of cancers. But the mechanisms underlying the decreased expression of FAM107B in cancers are not clear, the functional significance needs to be further clarified. Our previous findings from cDNA microarray showed that there are 179 differentially expressed genes after S100A4 inhibition in gastric cancer cells MGC803. FAM107B was an upregulated one among them. In the present study, we confirmed that FAM107B expression was upregulated in MGC803 cells after S100A4 inhibition by qRT-PCR. We demonstrated for the first time that FAM107B was downregulated by S100A4. The results from CCK-8 and transwell assay showed that FAM107B inhibition by siRNA led to significantly increased proliferation and migrating abilities of MGC803 cells, respectively, indicating that FAM107B plays important roles in inhibiting the proliferation and migration of MGC803 cells. The rescue experiment showed that FAM107B-siRNA transfection reversed the reduced proliferation and migration abilities induced by S100A4 inhibition in the cells. These findings suggest that, as a downstream effector, FAM107B at least partly mediates the effect of S100A4 on the proliferation and migration of MGC803 cells. In conclusion, we first provide experimental evidence suggesting that FAM107B was downregulated by S100A4 in gastric cancer MGC803 cells. And FAM107B at least partially mediates the biological effect of S100A4 in the cells.

Protein biomarkers for incident deep venous thrombosis in critically ill adolescents: An exploratory study

“…FAM107B is a heat‐shock–inducible tumor small protein that is expressed in a variety of tissues . Its expression is decreased in tumor tissues of the breast, thyroid, testis, and uterine cervix as well as the stomach and colon . Given the well‐established association between cancer and DVT, we would have expected the levels of FAM107B to be lower among adolescents with DVT than those without DVT, which was in contrast to our finding.…”

miR-3189-3p Mimics Enhance the Effects of S100A4 siRNA on the Inhibition of Proliferation and Migration of Gastric Cancer Cells by Targeting CFL2

“…RNAi was used to knock down S100A4 to study its effects on the properties of cancer cells. Specific knockdown of S100A4 resulted in cell responses in human GC and other cancer cells, such as decreased proliferation, migration, and invasion [ 7 , 9 , 27 , 28 , 29 ]. At the molecular level, the response involved a change in the expression of many genes.…”

“…At the molecular level, the response involved a change in the expression of many genes. After S100A4 knockdown in cancer cells, certain genes that inhibit proliferation and migration (e.g., FAM107B and E-cadherin ) were upregulated [ 27 , 30 ], while those genes that normally promote proliferation and migration (e.g., NF-κB, p65 and MMP2 ) were downregulated [ 7 , 31 ]. In addition, ectopic overexpression of S100A4 led to upregulation of oncogenic microRNA (miR)-155 expression in hepatocellular carcinoma cells, and an miR-155 inhibitor significantly attenuated the invasion-promoting effects of S100A4 [ 32 ].…”

LADON, a natural antisense transcript of NODAL, promotes an invasive behaviour in melanoma cells

“…All of these were up-regulated in A375∆E2 cells, suggesting a repressive role of LADON on their expression. Among the six proteins that had a fold change superior to 2 (Table 1B), 5 were overexpressed in A375∆E2 cells and turned out to be known tumor (FAM107B, ACPP) or metastasis (NDRG1) suppressors (Guo et al, 2017;Meeusen & Janssens, 2018;Sharma et al, 2017), or transcription factors known to activate these proteins (p65, also known as NF-κB regulatory subunit RELA, is an activator of ACPP) (Zelivianski et al, 2004). Conversely, the under-expressed protein PPP4R2 is a regulatory subunit of PPP4C, which is known to promote cancer cell growth and invasion (Hastie et al, 2000;X.…”