Tumor-promoting function of PIMREG in glioma by activating the β-catenin pathway

Wang, Dekang; Hu, Aili; Peng, Hao; Li, Dongbo; Zhang, Li

doi:10.1007/s13205-021-02922-5

Cited by 5 publications

(7 citation statements)

References 46 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…FAM64A not only augmented the transcriptional activity of FOXM1 but also regulated FOXM1 expression through an autoregulatory loop, thereby promoting the tumorigenesis of HNSCC. Previously, FAM64A expression was found to upregulate in, osteosarcoma (Jiang, Zhou, et al, 2020), breast cancer (Yao et al, 2019), glioma (Wang et al, 2021), lung cancer (Jiang et al, 2021), cholangiocarcinoma (Jiang, Li, et al, 2020), and HNSCC (Zhao et al, 2022), in line with our data. FAM64A mRNA expression was found to negatively associate with the purity and loss infiltration of immune cells in GC and no immunopositivity of FAM64A was observed in the infiltrative immune cells, which accounted for the consistency between our morphological and molecular findings.…”

Section: Effect Of Fam64a Expression On Chemoresistance and Lipid Dro...supporting

confidence: 92%

“…FAM64A downregulation in breast cancer cells decreased proliferation, migration, and epithelial–mesenchymal transition (EMT) (Yao et al, 2019), whereas FAM64A upregulation has the opposite effects (Jiang et al, 2019). Wang et al (2021) found that FAM64A overexpression significantly promoted proliferation, G 1 –S transition, migration, and invasion in glioma cells by activating the β‐catenin pathway. Zhang et al (2022) discovered that FAM64A could boost proliferation, avert apoptosis, and induce migration of colorectal cancer cells with the aid of the ERK/MAPK signaling pathway.…”

Section: Discussionmentioning

confidence: 99%

“…The paradoxical findings are interesting and worth further investigation.Using transgenic mice with postnatal FAM64A expression in cardiomyocytes,Hashimoto et al (2022) revealed that FAM64A could impede cardiomyocyte differentiation and cause heart dysfunction by repressing Klf15. FAM64A downregulation in breast cancer cells decreased proliferation, migration, and epithelial-mesenchymal transition (EMT)(Yao et al, 2019), whereas FAM64A upregulation has the opposite effects(Jiang et al, 2019) Wang et al (2021). found that FAM64A overexpression significantly promoted proliferation, G 1 -S transition, migration, and invasion in glioma cells by activating the β-catenin pathway Zhang et al (2022).…”

mentioning

confidence: 97%

See 2 more Smart Citations

FAM64A aggravates proliferation, invasion, lipid droplet formation, and chemoresistance in gastric cancer: A biomarker for aggressiveness and a gene therapy target

Yun

Yang

et al. 2023

Drug Development Research

Self Cite

View full text Add to dashboard Cite

FAM64A is a mitogen‐induced regulator of the metaphase and anaphase transition. Here, we found that FAM64A messenger RNA (mRNA) and protein expression levels were higher in gastric cancer tissue than in normal mucosa (p < .05). FAM64A methylation was negatively correlated with FAM64A mRNA expression (p < .05). The differentially expressed genes of FAM64A were mainly involved in digestion, potassium transporting or exchanging ATPase, contractile fibers, endopeptidase, and pancreatic secretion (p < .05). The FAM64A‐related genes were principally categorized into ubiquitin‐mediated proteolysis, cell cycle, chromosome segregation and mitosis, microtubule binding and organization, metabolism of amino acids, cytokine receptors, lipid droplet, central nervous system, and collagen trimer (p < .05). FAM64A protein expression was lower in normal gastric mucosa than intestinal metaplasia, adenoma, and primary cancer (p < .05), negatively correlated with older age, T stage, lymphatic and venous invasion, tumor, node, metastasis stage, and dedifferentiation (p < .05), and associated with a favorable overall survival of gastric cancer patients. FAM64A overexpression promoted proliferation, antiapoptosis, migration, invasion, and epithelial–mesenchymal transition via the EGFR/Akt/mTOR/NF‐κB, while the opposite effect was observed for FAM64A knockdown. FAM64A also induced chemoresistance directly or indirectly through lipid droplet formation via ING5. These results suggested that upregulation of FAM64A expression might induce aggressive phenotypes, leading to gastric carcinogenesis and its subsequent progression. Thus, FAM64A could be regarded as a prognosis biomarker and a target for gene therapy.

show abstract

Section: Effect Of Fam64a Expression On Chemoresistance and Lipid Dro...supporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 97%

See 1 more Smart Citation

FAM64A aggravates proliferation, invasion, lipid droplet formation, and chemoresistance in gastric cancer: A biomarker for aggressiveness and a gene therapy target

Yun

Yang

et al. 2023

Drug Development Research

Self Cite

View full text Add to dashboard Cite

show abstract

“…They form a complex with cyclin D1 to jointly regulate tumor proliferation, and this complex is becoming a new target for tumor therapy ( 23 , 24 ). Previous studies have reported that the knockdown of PIMREG can inhibit the proliferation of prostate cancer, glioma and breast cancer cells by prolonging G1 cell phase ( 9 , 13 , 14 ). In our study, the expression of cyclin D1 in ccRCC cells decreased significantly after silencing PIMREG .…”

Section: Discussionmentioning

confidence: 99%

“…PIMREG has been proved to control the transition of cell mitosis from metaphase to anaphase and regarded as a marker of proliferation (8). Recent studies have found that the upregulation of PIMREG expression is related to the poor prognosis of breast cancer, neuroblastoma, cholangiocarcinoma, osteosarcoma, glioma, prostate cancer and other cancers (9)(10)(11)(12)(13)(14). Although Wei et al and Zhu et al reported that PIMREG was related to overall survival (OS) and recurrence-free survival (RFS) of ccRCC and could be used as a biomarker of prognosis, we further verified the biological function of PIMREG in ccRCC through in vitro experiments and analyzed the relationship between PIMREG and immune infiltration and drug resistance (15,16).…”

Section: Introductionmentioning

confidence: 99%

PIMREG is a prognostic biomarker involved in immune microenvironment of clear cell renal cell carcinoma and associated with the transition from G1 phase to S phase

Yao

Lyu

et al. 2023

Front. Oncol.

View full text Add to dashboard Cite

BackgroundClear cell renal cell carcinoma (ccRCC) is one of the most common tumors in the world and affects human health seriously. PIMREG is a mitotic regulator which is essential to the metaphase-to-anaphase transition in cell cycle. Although PIMREG plays a crucial role in the malignant progression of tumors, there are few reports on its role in ccRCC.MethodsThe transcriptional expression profile and clinical data of PIMREG were downloaded from TCGA database and verified by qRT-PCR. Kaplan-Meier plotter was used to analyze the effect of PIMREG on overall survival (OS), disease specific survival (DSS) and progression-free interval (PFI) of patients with ccRCC. Univariable and multivariable Cox regression analysis were used to determine the independent prognostic factors of ccRCC. The effects of PIMREG on cell migration and invasion were detected by wound healing assay and transwell invasion assay, and CCK-8 assay, colony formation assay and cell cycle assay were used to detect the effect of PIMREG on cell proliferation. In addition, the changes in cell cycle related proteins were detected by western blot.ResultsPIMREG was highly expressed in human ccRCC and was positively correlated with pathologic stage, TNM stage and histologic grade. In addition, patients with high expression of PIMREG had a poor prognosis. Univariable and multivariable Cox regression analysis identified that PIMREG was an independent prognostic factor of ccRCC. Additionally, PIMREG was also closely related to immune cell infiltration. Experiments in vitro identified that the knockdown of PIMREG could significantly inhibit the proliferation, migration and invasion abilities of ccRCC. The expression of cyclin D1, CDK4 and CDK6 was also significantly reduced after PIMREG knockdown.ConclusionsPIMREG plays a vital role in the development of ccRCC and may become a potential therapeutic target in the future.

show abstract

Cell Cycle-Related FAM64A Could be Activated by TGF-β Signaling to Promote Glioma Progression

Zhang

et al. 2023

Cell Mol Neurobiol

View full text Add to dashboard Cite

BackgroundFAM64A has been found to promote tumor cell proliferation in various tumors. However, the regulatory mechanism and clinical signi cance of FAM64A in gliomas still remain unclear. MethodsFAM64A expression in gliomas with different grades was determined by TCGA database mining and immunoblotting assay. FAM64A silenced U87 cells were constructed with shRNA, and cell proliferation, migration, and cell cycle and were detected by CCK8 assay, scratch assay, and ow cytometry respectively. Intercellular crosstalk analysis and transcription factor prediction were performed to query the potential regulatory mechanisms. TGF-b and its downstream transcription factors were detected in glioma samples with different grades to validate the regulatory roles of TGF-b signaling. ResultsFAM64A was highly expressed in glioblastoma and associated with a poor prognosis. FAM64A silenced U87 cell lines displayed disrupted proliferation and migration ability. More cells would be stuck in the S phase. Expression pro les at the single-cell resolution further indicated that FAM64A could play a role in a cell-cycle-dependent way to promote the proliferation of glioma cells. FAM64A expression could be induced by TGF-β signal. And colocalization of SMAD4 and FAM64A could be observed in high-grade glioma tissues. ConclusionsFAM64A could serve as a malignant biomarker in gliomas, and it could be induced via TGF-β pathway activation., which could explain the crosstalk between glioma cells and also the microenvironment.

show abstract

Tumor-promoting function of PIMREG in glioma by activating the β-catenin pathway

Cited by 5 publications

References 46 publications

FAM64A aggravates proliferation, invasion, lipid droplet formation, and chemoresistance in gastric cancer: A biomarker for aggressiveness and a gene therapy target

FAM64A aggravates proliferation, invasion, lipid droplet formation, and chemoresistance in gastric cancer: A biomarker for aggressiveness and a gene therapy target

PIMREG is a prognostic biomarker involved in immune microenvironment of clear cell renal cell carcinoma and associated with the transition from G1 phase to S phase

Cell Cycle-Related FAM64A Could be Activated by TGF-β Signaling to Promote Glioma Progression

Contact Info

Product

Resources

About