FAM172A modulates apoptosis and proliferation of colon cancer cells via STAT1 binding to its promoter

Qian, Kai; Zhang, Jinqian; Lu, Jing-Bo; Liu, Wenjun; Yao, Xiang; Chen, Qing; Lu, Shun; Liu, Hao

doi:10.3892/or.2015.4485

Cited by 14 publications

(18 citation statements)

References 20 publications

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“…As a protein of 416 amino acid, FAM172A belongs to the UPF0528 family and its protein-coding gene is located in human chromosome 5 (9). Our previous research showed that FAM172A expression had a lower expression in CRC tissues of patients with metastasis compared with CRC tissues of patients without metastasis (11). However, relevant studies of FAM172A and its more unknown functions in CRC are still scarce.…”

Section: Discussionmentioning

confidence: 97%

“…Our prior studies showed that overexpression of FAM172A inhibited the migrational capability and cell invasiveness of CRC cell lines by suppressing the expression of MMPs (11). To further explore the biological functions of FAM172A regulated by miR-27a in LoVo and SW480 cell lines, we determine the effect of miR-27a on cell poliferation, migration and invasion.…”

Section: Discussionmentioning

confidence: 99%

“…Our previous study showed that FAM172A expression in cancerous tissues was obviously lower compared with adjacent tissues of CRC cells by using immunohistochemical staining (10). In addition, our other past results showed that FAM172A could promote apoptosis and inhibit proliferation of CRC cell lines by flow cytometry and STAT1 could upregulate the expression of FAM172A when it was combined with the promoter region of FAM172A, indicating that FAM172A might be a novel tumor-suppressor gene (11). However, more molecular mechanisms of FAM172A underlying this process are still to be elucidated.…”

Section: Introductionmentioning

confidence: 96%

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miR-27a promotes proliferation, migration, and invasion of colorectal cancer by targeting FAM172A and acts as a diagnostic and prognostic biomarker

et al. 2017

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Accumulating evidence shows that mircroRNAs (miRNAs) play a crucial role in the development of colorectal cancer. In our previous study, FAM172A was demonstrated to be a novel tumor suppressor gene in CRC. Therefore, the aim of the present study was to identify whether the miR‑27a could be a diagnostic and prognostic marker and the regulatory relationships between miR‑27a and FAM172A. We demonstrated high levels of miR‑27a expression in tissues of patients with CRC as well as in CRC cell lines. There was a positive correlation between the levels of miR‑27a and the poor overall survival of patients with CRC. Furthermore, elevated levels of miR‑27a expression were associated with TNM stage and distant metastasis. Increased expression or inhibition of miR‑27a promoted or inhibited the metastasis of CRC cell lines, respectively. Moreover, we showed that miR‑27a directly targets the 3'-untranslated region of FAM172A mRNA by using a dual-luciferase assay. Increased or decreased expression of FAM172A expression was observed when miR‑27a expression was inhibited or elevated in the CRC cells, respectively. In summary, our study showed that miR‑27a expression is a diagnostic and prognostic marker and correlates with overall survival of patients with CRC. Therefore, it may be a therapeutic approach for preventing metastasis of CRC to inhibit expression of miR‑27a or increase expression of FAM172A.

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Section: Discussionmentioning

confidence: 97%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 96%

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miR-27a promotes proliferation, migration, and invasion of colorectal cancer by targeting FAM172A and acts as a diagnostic and prognostic biomarker

et al. 2017

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“…Cui et al has also reported in a work with a colorectal cancer model that FAM172A might inhibit the growth and invasion of colorectal cancer cells and the mechanism involved activation of ERS signaling [24]. Qian et al demonstrated that FAM172A was upregulated by the STAT1 transcription factor and also downregulated, thus modulating apoptosis and the proliferation process of colon cancer cells (human LoVo and SW480 cells) [33]. Similar in line with the results in our studies, Wang and Tai demonstrated that high expression levels of MAPK, phosphorylated MAPK, and phosphorylated MEK1/2 were found in tumors of HCC patients [16].…”

Section: Discussionmentioning

confidence: 93%

The Effect of Protein FAM172A on Proliferation in HepG2 Cells and Investigation of the Possible Molecular Mechanism

Zhao

Wang

Liu

et al. 2019

Analytical Cellular Pathology

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Background. In our previous study, we found that the FAM172A recombinant protein could promote proliferation of L02 cells. However, the underlying mechanisms are still unknown. The present study was aimed at investigating the effect of FAM172A on proliferation of HepG2 cells and exploring the possible molecular mechanisms and its role in hepatocellular carcinoma (HCC). Methods. Cell proliferation was measured by MTT assay. Western blot test was carried out to investigate the mechanism. Rabbit antibodies against FAM172A and membrane proteins isolated from lysate of HepG2 cell were coprecipitated and the resultant precipitates were analyzed by mass spectrum. Results. The MTT assay showed that recombinant protein FAM172A isoform 1 (FAM172A-1) could induce HepG2 cell proliferation at the concentration of 10-100 ng/mL, while protein FAM172A isoform 3 (FAM172A-3) was at the concentration of 80-100 ng/mL. Western blot demonstrated that both FAM172A-1 and FAM172A-3 could activate the mitogen-activated protein kinase/extracellular signal-regulated protein kinase (MAPK/ERK) pathway and the phosphatidylinositol 3-kinase/threonine-protein kinase (PI3K/Akt) pathway. Mass spectrum analysis suggested that there were some membrane proteins interacting with FAM172A. Several candidate interacting proteins might mediate proliferation signals induced by FAM172A recombinant protein, including seven membrane proteins. Conclusion. In conclusion, FAM172A recombinant protein could induce proliferation of HepG2 cells, in which the MAPK/ERK and PI3K/Akt signaling pathways might be involved. The role of FAM172A in HepG2 cell proliferation also indicated its possible involvement in HCC. The receptor of FAM172A on cells still needs to be exploited.

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“…3E), and F ( Effect of tea tree oil on inflammatory factors and apoptotic factors in the LPS-induced mastitis model TNF-α and IL-6 are inflammatory factors related to the inflammatory response (20). STAT1 is related to apoptosis (21). Compared with the blank group, TNF-α and IL-6 were expressed more than 15 times higher in response to LPS treatment at a concentration of 200 µg/ml.…”

Section: Effect Of Tea Tree Oil On Lps-induced Bmecsmentioning

confidence: 87%

Tea tree oil prevents mastitis-associated inflammation in lipopolysaccharide-stimulated bovine mammary epithelial cells

Chen

Zhang

Zhou

et al. 2020

Preprint

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Background Effective prevention and treatment of cow mastitis can provide a good guarantee for the healthy growth of cows and the qualified production of dairy products. The main purpose of this study was to explore the effect of tea tree oil on lipopolysaccharide (LPS) -induced mastitis in dairy cows, and the key gene in LPS -stimulated bovine mammary epithelial cells (BMECs) was identified. Results In this study, a model of mastitis induced by LPS was constructed, to which tea tree oil and LPS were added. The protective effects of tea tree oil on LPS-induced mastitis in BMECs were verified by the CCK-8 method, flow cytometry, real-time fluorescence quantitative detection, ELISA and other methods. The results showed that LPS at a concentration of 200 μg/ml could reduce the proliferative activity of the cells, induce a high proportion of apoptosis, and promote the expression of TNF-α, IL-6 and STAT1. Upon addition of tea tree oil, the proportion of apoptosis was reduced, and the expression of NF-κB, MAPK and caspase-3 was inhibited. Mammary epithelial cells were compared under control and LPS-treatment conditions and analyzed by second-generation sequencing. A total of 1270 mRNAs were identified as differentially expressed, of which 787 genes were upregulated and 483 were downregulated. These differentially expressed genes include TNF - α, IL6, STAT1, mapk4, etc. H&E staining and immunohistochemistry were used to verify the function of candidate genes. TNF-α and IL6 were observed to play important roles in mediating the preventive effect of tea tree oil on mastitis in LPS-stimulated bovine mammary epithelial cells. Conclusions The results showed that tea tree oil had a protective effect against LPS-induced mastitis. TNF - α and IL6 may be the marker genes of LPS-induced mastitis which provided a theoretical basis and experimental support for further research to determine new strategies for the prevention and treatment of mastitis and improvement of milk quality.

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FAM172A modulates apoptosis and proliferation of colon cancer cells via STAT1 binding to its promoter

Cited by 14 publications

References 20 publications

miR-27a promotes proliferation, migration, and invasion of colorectal cancer by targeting FAM172A and acts as a diagnostic and prognostic biomarker

miR-27a promotes proliferation, migration, and invasion of colorectal cancer by targeting FAM172A and acts as a diagnostic and prognostic biomarker

The Effect of Protein FAM172A on Proliferation in HepG2 Cells and Investigation of the Possible Molecular Mechanism

Tea tree oil prevents mastitis-associated inflammation in lipopolysaccharide-stimulated bovine mammary epithelial cells

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