FAM64A Promotes Osteosarcoma Cell Growth and Metastasis and Is Mediated by miR-493

Jiang, Ying; Zhou, Chunlei; Gao, Qiang; Yin, Zhiqi; Wang, Jingwen; Hong, Ming; Yan, Jun

doi:10.1155/2020/2518297

Cited by 9 publications

(8 citation statements)

References 16 publications

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“…This work showed that the PIMREG gene was highly expressed in 20 cancers, and IHC results confirmed this trend at protein level. The results of CHOL, COAD, SARC, BRCA, and LUAD resembled the results of previous studies ( Jiang Y. et al, 2020 ; Jiang Z.M. et al, 2020 ; Mizuno et al, 2020 ; Xu Z.S.…”

Section: Discussionsupporting

confidence: 89%

Pan-Cancer Analysis of PIMREG as a Biomarker for the Prognostic and Immunological Role

Zhu

et al. 2021

Front. Genet.

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Phosphatidylinositol binding clathrin assembly protein interacting mitotic regulator (PIMREG) localizes to the nucleus and can significantly elevate the nuclear localization of clathrin assembly lymphomedullary leukocythemia gene. Although there is some evidence to support an important action for PIMREG in the occurrence and development of certain cancers, currently no pan-cancer analysis of PIMREG is available. Therefore, we intended to estimate the prognostic predictive value of PIMREG and to explore its potential immune function in 33 cancer types. By using a series of bioinformatics approaches, we extracted and analyzed datasets from Oncomine, The Cancer Genome Atlas, Cancer Cell Lineage Encyclopedia (CCLE) and the Human Protein Atlas (HPA), to explore the underlying carcinogenesis of PIMREG, including relevance of PIMREG to prognosis, microsatellite instability (MSI), tumor mutation burden (TMB), tumor microenvironment (TME) and infiltration of immune cells in various types of cancer. Our findings indicate that PIMREG is highly expressed in at least 24 types of cancer, and is negatively correlated with prognosis in major cancer types. In addition, PIMREG expression was correlated with TMB in 24 cancers and with MSI in 10 cancers. We revealed that PIMREG is co-expressed with genes encoding major histocompatibility complex, immune activation, immune suppression, chemokine and chemokine receptors. We also found that the different roles of PIMREG in the infiltration of different immune cell types in different tumors. PIMREG can potentially influence the etiology or pathogenesis of cancer by acting on immune-related pathways, chemokine signaling pathway, regulation of autophagy, RIG-I like receptor signaling pathway, antigen processing and presentation, FC epsilon RI pathway, complement and coagulation cascades, T cell receptor pathway, NK cell mediated cytotoxicity and other immune-related pathways. Our study suggests that PIMREG can be applied as a prognostic marker in a variety of malignancies because of its role in tumorigenesis and immune infiltration.

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Section: Discussionsupporting

confidence: 89%

Pan-Cancer Analysis of PIMREG as a Biomarker for the Prognostic and Immunological Role

Zhu

et al. 2021

Front. Genet.

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“… 22 Ectopic expression of FAM64A enhanced the proliferation, migration and invasion capabilities of osteosarcoma cells, and the tumor promoting effects of FAM64A were mediated by miR-493. 23 FAM64A downregulation was also reported to suppress the proliferation of lung cancer cells. 24 Although FAM64A is closely correlated with the malignant behaviors of cancer cells, the detailed molecular mechanisms are poorly understood.…”

Section: Discussionmentioning

confidence: 96%

FAM64A promotes HNSCC tumorigenesis by mediating transcriptional autoregulation of FOXM1

et al. 2022

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Head and neck squamous cell carcinoma (HNSCC) still lacks effective targeted treatment. Therefore, exploring novel and robust molecular targets is critical for improving the clinical outcome of HNSCC. Here, we reported that the expression levels of family with sequence similarity 64, member A (FAM64A) were significantly higher in HNSCC tissues and cell lines. In addition, FAM64A overexpression was found to be strongly associated with an unfavorable prognosis of HNSCC. Both in vitro and in vivo evidence showed that FAM64A depletion suppressed the malignant activities of HNSCC cells, and vice versa. Moreover, we found that the FAM64A level was progressively increased from normal to dysplastic to cancerous tissues in a carcinogenic 4-nitroquinoline-1-oxide mouse model. Mechanistically, a physical interaction was found between FAM64A and forkhead box protein M1 (FOXM1) in HNSCC cells. FAM64A promoted HNSCC tumorigenesis not only by enhancing the transcriptional activity of FOXM1, but also, more importantly, by modulating FOXM1 expression via the autoregulation loop. Furthermore, a positive correlation between FAM64A and FOXM1 was found in multiple independent cohorts. Taken together, our findings reveal a previously unknown mechanism behind the activation of FOXM1 in HNSCC, and FAM64A might be a promising molecular therapeutic target for treating HNSCC.

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“…In addition, we found that FAM64A promoted not only the proliferation and migration/invasion of PCa cells but also the cell cycle, which suggests that FAM64A may be closely related to the occurrence and progression of PCa. Several studies have shown that overexpression of FAM64A accelerated the proliferation, migration, and invasion of esophageal cancer cells, breast cancer, pancreatic cancer, lymphoma, and other tumor tissues than normal tissues [ 7 – 9 , 12 ]. Arcangelo et al reported that FAM64A plays a role in controlling cell proliferation and can be regarded as a sign of proliferation [ 13 ].…”

Section: Discussionmentioning

confidence: 99%

FAM64A is an androgen receptor-regulated feedback tumor promoter in prostate cancer

Zhou

et al. 2021

Cell Death Dis

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Endocrine therapy for prostate cancer (PCa) mainly inhibits androgen receptor (AR) signaling, due to increased androgen synthesis and AR changes, PCa evolved into castration-resistant prostate cancer (CRPC). The function of Family With Sequence Similarity 64 Member A (FAM64A) and its association with prostate cancer has not been reported. In our research, we first reported that FAM64A is up-regulated and positively associated with poor prognosis of patients with prostate cancer (PCa) by TCGA database and immunohistochemistry staining. Moreover, knockdown of FAM64A significantly suppressed the proliferation, migration, invasion, and cell cycle of PCa cells in vitro. Mechanistically, FAM64A expression was increased by dihydrotestosterone (DHT) through direct binding of AR to FAM64A promoter, and notably promoted the proliferation, migration, invasion, and cell cycle of androgen-dependent cell line of PCa. In addition, abnormal expression of FAM64A affects the immune and interferon signaling pathway of PCa cells. In conclusion, FAM64A was up-regulated by AR through directly binding to its specific promoter region to promote the development of PCa, and was associated with the immune mechanism and interferon signaling pathway, which provided a better understanding and a new potential for treating PCa.

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FAM64A Promotes Osteosarcoma Cell Growth and Metastasis and Is Mediated by miR-493

Cited by 9 publications

References 16 publications

Pan-Cancer Analysis of PIMREG as a Biomarker for the Prognostic and Immunological Role

Pan-Cancer Analysis of PIMREG as a Biomarker for the Prognostic and Immunological Role

FAM64A promotes HNSCC tumorigenesis by mediating transcriptional autoregulation of FOXM1

FAM64A is an androgen receptor-regulated feedback tumor promoter in prostate cancer

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