FGD1 exhibits oncogenic properties in hepatocellular carcinoma through regulating cell morphology, autophagy and mitochondrial function

Zeng, Yonglian; Guo, Zhenya; Hu, Zhigao; Liu, Mingjiang; Chen, Yubing; Chen, Shilian; Peng, Bo; Zhang, Peng; Wu, Zhan He; Luo, Haiwei; Zhong, Fan; Jiang, Keqing; Lü, Yi; Yuan, Guandou; He, Songqing

doi:10.1016/j.biopha.2020.110029

Cited by 15 publications

(18 citation statements)

References 36 publications

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“…VAV2 promotes Rac1 and Cdc42 activation, leading to lamellipodia formation, facilitating metastasis of HCC cells. Interestingly, miRNA-195 suppresses angiogenesis and metastasis of HCC by inhibiting the expression of VEGF, VAV2 and Cdc42 [98] .…”

Section: Rho Gefs In Liver Cancermentioning

confidence: 99%

Contribution of C3G and other GEFs to liver cancer development and progression

Porrás¹,

Sequera²,

Bragado³

et al. 2021

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Primary liver cancers constitute the fourth leading cause of cancer mortality worldwide, due to their high morbidity, late diagnosis and lack of effective treatments. Hepatocellular carcinoma (HCC) represents 80% and cholangiocarcinoma (CCA) 15% of liver cancers. Several genetic and epigenetic gene alterations (e.g., TERT, TP53 or CTNNB1) are HCC drivers, although many additional gene alterations contribute to HCC initiation and/or progression. Rho and Ras GTPases have been widely implicated in tumorigenesis and their activators (GEFs) have recently emerged as putative key players in liver cancer. The Ras GEF, C3G (RAPGEF1), a GEF mainly for Rap proteins, has recently been uncovered as a relevant gene in HCC. Its upregulation promotes tumor growth, although a decrease in C3G levels favors migration/invasion and lung metastasis. Rap1A/1B/2A/2B are overexpressed in HCC tumors, but their effects are controversial and not equivalent to those of C3G. The C3G partner, CRKL, is also overexpressed in HCC, promoting proliferation, migration and invasion. Various Rho GEFs are also deregulated in liver cancer. Tiam1 and Tiam2 expression is upregulated in HCC, promoting proliferation, migration and metastasis. In addition, ARHGEF-10L/9/19/39 are overexpressed in HCC tumors, facilitating migration, invasion, metastasis and proliferation. Another Rho GEF, Vav2, is also involved in metastasis. Little is known about the participation of these GEFs and GTPases in CCA. However, analysis of cancer databases uncovered deregulations or genetic alterations in several of these genes, in both CCA and HCC. Hence, GEFs

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Section: Rho Gefs In Liver Cancermentioning

confidence: 99%

Contribution of C3G and other GEFs to liver cancer development and progression

Porrás¹,

Sequera²,

Bragado³

et al. 2021

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“…Under pathological condition, abnormal mitosis of mitochondria was related to the development of tumors [10,11]. At present, studies found that the expression of MTFR2 in breast cancer tissue was increased, and was correlated to the clinicopathological features and poor prognosis of patients.…”

Section: Discussionmentioning

confidence: 88%

Evaluation of clinical value and potential mechanism of MTFR2 in lung adenocarcinoma via bioinformatics

Chen

Tang

et al. 2020

Preprint

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Background Mitochondrial fission regulator 2 (MTFR2) was involved in the progression and development of various cancers. However, the relationship between MTFR2 with lung adenocarcinoma (LUAD) had not been reported. Herein, this study analyzed the clinical significance and potential mechanisms of MTFR2 in LUAD via bioinformatic tools. Results We found that the level of MTFR2 was increased, and correlated with sex, age, smoking history, neoplasm staging, histological subtype and TP53 mutation status in LUAD patients. Kaplan-Meier survival analysis showed LUAD patients with increased MTFR2 had a poor prognosis. In addition, univariate COX regression analysis showed neoplasm staging, T stage, distant metastasis and MTFR2 level were risk factors for the prognosis of LUAD. A total of 1127 genes were coexpressed with MTFR2, including 840 positive and 208 negative related genes. KEGG and GSEA found that MTFR2 participated in the progression of LUAD by affecting cell cycle, DNA replication, homologous recombination, p53 signaling pathway and other mechanisms. The top 10 coexpressed genes, namely CDK1, CDC20, CCNB1, PLK1, CCNA2, AURKB, CCNB2, BUB1B, MAD2L1 and BUB1 were highly expressed, and were associated with poor prognosis in LUAD. Conclusions Consequently, we elucidated MTFR2 was a biomarker for diagnosis and poor prognosis in LUAD, and might participate in the progression of LUAD via affecting cell cycle, DNA replication, homologous recombination and p53 signaling pathway.

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“…MTFR2 played an vital role in promoting the division of mitochondria in cells. Under pathological condition, abnormal mitosis of mitochondria was related to the development of tumors [10,11]. At present, studies found that the expression of MTFR2 in breast cancer tissue was increased, and was correlated to the clinicopathological features and poor prognosis of patients.…”

Section: Screening Of Mtfr2 Co-expressed Genesmentioning

confidence: 88%

“…Mitochondrial ssion regulator 2 (MTFR2), also known as FAM54A, was located on the 6q23.2 chromosome and belonged to the MTFR family. Abnormal mitosis of mitochondria was related to the pathogenesis of many diseases, and it promoted the development, and was correlated to occurrence and prognosis of several tumors [7][8][9][10][11]. MTFR2 was up-regulated in breast cancer and was related to age, lymph node metastasis, and prognosis of HER2 positive breast cancer patients.…”

Section: Introductionmentioning

confidence: 99%

Evaluation of Clinical Value and Potential Mechanism of MTFR2 in Lung Adenocarcinoma via Bioinformatics

Chen

Tang

et al. 2021

Preprint

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Background: Mitochondrial fission regulator 2 (MTFR2) was involved in the progression and development of various cancers. However, the relationship between MTFR2 with lung adenocarcinoma (LUAD) had not been reported. Herein, this study analyzed the clinical significance and potential mechanisms of MTFR2 in LUAD via bioinformatics tools.Results: We found that the level of MTFR2 was increased, and correlated with sex, age, smoking history, neoplasm staging, histological subtype and TP53 mutation status in LUAD patients. Kaplan-Meier survival analysis showed LUAD patients with increased MTFR2 had a poor prognosis. In addition, univariate COX regression analysis showed neoplasm staging, T stage, distant metastasis and MTFR2 level were risk factors for the prognosis of LUAD. A total of 1127 genes were coexpressed with MTFR2, including 840 positive and 208 negative related genes. KEGG and GSEA found that MTFR2 participated in the progression of LUAD by affecting cell cycle, DNA replication, homologous recombination, p53 signaling pathway and other mechanisms. The top 10 coexpressed genes, namely CDK1, CDC20, CCNB1, PLK1, CCNA2, AURKB, CCNB2, BUB1B, MAD2L1 and BUB1 were highly expressed, and were associated with poor prognosis in LUAD. Conclusions: Consequently, we elucidated MTFR2 was a biomarker for diagnosis and poor prognosis in LUAD, and might participate in the progression of LUAD via affecting cell cycle, DNA replication, homologous recombination and p53 signaling pathway.

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FGD1 exhibits oncogenic properties in hepatocellular carcinoma through regulating cell morphology, autophagy and mitochondrial function

Cited by 15 publications

References 36 publications

Contribution of C3G and other GEFs to liver cancer development and progression

Contribution of C3G and other GEFs to liver cancer development and progression

Evaluation of clinical value and potential mechanism of MTFR2 in lung adenocarcinoma via bioinformatics

Evaluation of Clinical Value and Potential Mechanism of MTFR2 in Lung Adenocarcinoma via Bioinformatics

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