FAM83A is amplified and promotes cancer stem cell-like traits and chemoresistance in pancreatic cancer

Chen, S; Huang, Jian; Liu, Zhiyong; Liang, Qi; Zhang, N; Jin, Y.

doi:10.1038/oncsis.2017.3

Cited by 74 publications

(72 citation statements)

References 45 publications

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“…Concordantly, researches proved that FAM83A presented high expression in several other human cancers, such as in breast, testis, bladder and pancreatic cancer [12,21,22]. Moreover, high expression level of FAM83A in pancreatic cancer was correlated with poorer survival [12]. When exploring the mechanism of FAM83A up-regulation, its genomic locus is of interest.…”

Section: Discussionmentioning

confidence: 92%

“…Recently it was found that the DUF1669 domain of FAM83 family proteins anchored casein kinase 1 isoforms which were implicated in the regulation of many cellular processes [11]. FAM83A (originally named BJ-TSA-9) is highly expressed across tumor types [7,12,13]. In pancreatic cancer, FAM83A is amplified and promotes cancer stem cell-like traits [12].…”

Section: Introductionmentioning

confidence: 99%

“…FAM83A (originally named BJ-TSA-9) is highly expressed across tumor types [7,12,13]. In pancreatic cancer, FAM83A is amplified and promotes cancer stem cell-like traits [12]. In breast cancer cells, silencing FAM83A markedly decreased cell proliferation and invasion and elevated expression of apoptosis markers [7,14].…”

Section: Introductionmentioning

confidence: 99%

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FAM83A is amplified and promotes tumorigenicity in non-small cell lung cancer via ERK and PI3K/Akt/mTOR pathways

Hu¹,

Wang²,

Wang³

et al. 2020

Int. J. Med. Sci.

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Family with sequence similarity 83A (FAM83A) is a newly-found over-expressed oncogene in several types of cancers and associates with poor prognosis. However, the role that FAM83A may play in the carcinogenesis of non-small cell lung cancer (NSCLC) still needs to be defined. The present study aimed to investigate the function of FAM83A in NSCLC progression and to investigate the possible mechanism. Analysis of Gene Expression Omnibus (GEO) database and rt-PCR showed up-regulated expression of FAM83A in NSCLC. GEO and the Cancer Genome Atlas (TCGA) data analysis revealed that high expression level of FAM83A in NSCLC was associated with poor prognosis. In vitro experiments showed that depleting FAM83A by siRNA/shRNA significantly inhibited cell proliferation and induced cell apoptosis. Cell motility was also retarded after silencing FAM83A, as demonstrated by Transwell assay. FAM83A depletion in A549 cells also inhibited subcutaneous tumor growth and lung metastasis in vivo. Western blotting showed that silencing FAM83A decreased the phosphorylation of ERK and PI3K/Akt/mTOR. On the other hand, overexpressing FAM83A in vitro enhanced cell proliferation and invasiveness, which was repressed by PI3K inhibitor and ERK inhibitor separately. Taken together, our study suggests that FAM83A promotes tumorigenesis of NSCLC at least partly via ERK and PI3K/Akt/mTOR pathways, making it a promising therapeutic target.

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Section: Discussionmentioning

confidence: 92%

Section: Introductionmentioning

confidence: 99%

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FAM83A is amplified and promotes tumorigenicity in non-small cell lung cancer via ERK and PI3K/Akt/mTOR pathways

Hu¹,

Wang²,

Wang³

et al. 2020

Int. J. Med. Sci.

View full text Add to dashboard Cite

show abstract

“…FAM83A is involved in regulating a variety of different tumor-related signaling pathways, including the EGFR, RAS/RAF/MEK/ERK, and PI3K/AKT/mTOR pathways (3,4). The overexpression of FAM83A has been shown in lung, breast, testicular, and bladder cancers and is associated with promoting the development of cancers (7)(8)(9)(19)(20)(21)(22). Li et al (3) reported that FAM83A is highly expressed in lung cancer tissues, especially LUAD.…”

Section: Discussionmentioning

confidence: 99%

FAM83A Promotes Lung Cancer Progression by Regulating the Wnt and Hippo Signaling Pathways and Indicates Poor Prognosis

Zheng

Lei

et al. 2020

Front. Oncol.

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FAM83A (family with sequence similarity 83, member A) has been found to be highly expressed in cancers. The purpose of this study was to clarify the role and mechanism of FAM83A in lung cancers. The expression of FAM83A in lung cancer cells was enhanced by gene transfection or knocked down by small interfering RNA interference. The key proteins of the Wnt signaling pathway, the Hippo signaling pathway, and epithelial-mesenchymal transition (EMT) were examined using Western blot. The proliferation and invasion of lung cancer cells were examined using cell proliferation, colony formation, and invasion assays. The expression of FAM83A in lung cancer tissues was significantly increased and was correlated with advanced tumor-node-metastasis (TNM) stage and poor prognosis. Overexpression of FAM83A enhanced the proliferation, colony formation, and invasion of lung cancer cells. Meanwhile, FAM83A overexpression increased the expression of active β-catenin and Wnt target genes and the activity of EMT. Furthermore, in FAM83A-overexpressed cells, the activity of Hippo pathway was downregulated, whereas the expression of yes-associated protein (YAP) and its downstream targets cyclin E and CTGF were upregulated. The inhibitor of the Wnt signaling pathway, XAV-939, reversed the promoting effect of FAM83A on YAP, cyclin E, and CTGF. On knocking down the expression of FAM83A, we obtained the opposite results. However, the inhibitor of GSK3β, CHIR-99021, restored the expression of YAP, cyclin E, and CTGF after FAM83A was knocked down. FAM83A is highly expressed in lung cancers and correlated with advanced TNM stage and poor prognosis. FAM83A promotes the proliferation and invasion of lung cancer cells by regulating the Wnt and Hippo signaling pathways and EMT process.

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“…Drug resistance is identified as a major obstacle in tumor chemotherapy, and miRNAs have been reported to serve critical roles in this process (17)(18)(19)(20)(21)(22)(23). To date, several studies have identified that miR-149 exerts a critical function in numerous types of tumors.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-149 suppresses the proliferation and increases the sensitivity of ovarian cancer cells to cisplatin by targeting X-linked inhibitor of apoptosis

et al. 2018

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Abstract. Currently, ovarian cancer is identified as one of the leading causes of cancer-associated mortality in females. Despite numerous efforts that were made on developing novel treatments for ovarian cancer, the survival rate remains unsatisfactory. Considering the important regulatory role of miRNAs in different types of cancer, the present study aims to identify a novel therapeutic target for treatment of ovarian cancer. The expression of miR-149 was detected using reverse transcription-quantitative polymerase chain reaction in cancerous and normal cells. Furthermore, the effects of miR-149 on ovarian cancer cell activities were investigated using MTT assay, colony formation, flow cytometry and western blotting analysis. In the present study, it was revealed that microRNA (miR)-149 was significantly downregulated in ovarian cancer tissues and cell lines, and that the miR-149 expression was correlated with the patient prognosis. In addition, it was observed that forced expression of miR-149 increased the sensitivity of ovarian cancer cell to cisplatin. Based on bioinformatics analysis and luciferase assay, X-linked inhibitor of apoptosis (XIAP) was identified as a direct target gene of miR-149 in ovarian cancer cells. It was also demonstrated that XIAP expression was upregulated in the ovarian cancer tissues and cell lines, while it was negatively correlated with miR-149 in these tissues and cells. Furthermore, results revealed that ectopic expression of XIAP was able to abolish the miR-149-enhanced cell sensitivity to cisplatin. In conclusion, the present study revealed that miR-149 functioned as a tumor suppressor in the progression of ovarian cancer, increasing the sensitivity of ovarian cancer cells to cisplatin treatment.

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FAM83A is amplified and promotes cancer stem cell-like traits and chemoresistance in pancreatic cancer

Cited by 74 publications

References 45 publications

FAM83A is amplified and promotes tumorigenicity in non-small cell lung cancer via ERK and PI3K/Akt/mTOR pathways

FAM83A is amplified and promotes tumorigenicity in non-small cell lung cancer via ERK and PI3K/Akt/mTOR pathways

FAM83A Promotes Lung Cancer Progression by Regulating the Wnt and Hippo Signaling Pathways and Indicates Poor Prognosis

MicroRNA-149 suppresses the proliferation and increases the sensitivity of ovarian cancer cells to cisplatin by targeting X-linked inhibitor of apoptosis

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