&lt;p&gt;FAM111B, a direct target of p53, promotes the malignant process of lung adenocarcinoma&lt;/p&gt;

Sun, Haoliang; Liu, Kaichao; Huang, Jianfeng; Sun, Qi; Shao, Chengchen; Lin, Xu; Shen, Yi; Ren, Bingzhong

doi:10.2147/ott.s190934

Cited by 37 publications

(71 citation statements)

References 27 publications

(26 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Interfering with FAM111B inhibited the proliferation, cell cycle arrest and migration of LUAD cells and the ability of tumor formation in nude mice, but induced apoptosis. FAM111B might regulate the growth of LUAD through p53 signaling pathway, inhibit the expression of BAG3 and BCL2, and play an important role in cell cycle and apoptosis [21]. In present study, we found that MTFR2 coexpressed genes were mainly involved in cell cycle, DNA replication, homologous recombination, p53 signaling pathway and other signaling pathways by KEGG.…”

Section: Screening Of Mtfr2 Co-expressed Genessupporting

confidence: 48%

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

Chen

Tang

et al. 2021

Preprint

View full text Add to dashboard Cite

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.

show abstract

Section: Screening Of Mtfr2 Co-expressed Genessupporting

confidence: 48%

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

Chen

Tang

et al. 2021

Preprint

View full text Add to dashboard Cite

show abstract

“…3A ). In the list of lung_NSC cell lines with high expression of FAM83A, the common LUAD cell line, NCIH1650, has been used for research in a previous study ( 18 ) and was selected for subsequent experiments ( Fig. 3B ).…”

Section: Resultsmentioning

confidence: 99%

FAM83A and FAM83A‑AS1 both play oncogenic roles in lung adenocarcinoma

Wang

Yao

et al. 2021

Oncol Lett

Self Cite

View full text Add to dashboard Cite

Lung adenocarcinoma (LUAD) is the most common subtype of lung cancer. Nevertheless, the detailed molecular mechanisms of the progression of LUAD remain largely unknown. The present bioinformatics analysis reported that FAM83A and FAM83A-AS1 were upregulated in LUAD tissues and associated with prognosis in patients with LUAD. The purpose of the current study was to investigate the role of FAM83A and its antisense long non-coding (lnc)RNA FAM83A-AS1 in LUAD. Gene Expression Profiling Interactive Analysis was used to screen for potential oncogenes in LUAD and to analyze the clinical significance of FAM83A and FAM83A-AS1. Small interfering RNAs were constructed and transfected into LUAD cells to knock down the expression of FAM83A and FAM83A-AS1. EdU, Cell Counting Kit-8, Transwell and Matrigel assays were performed to detect the proliferation, migration and invasion of LUAD cells. The interaction between FAM83A-AS1, microRNA (miR)-495-3p and FAM83A was explored using a luciferase reporter assay. FAM83A and FAM83A-AS1 were both overexpressed in LUAD tissues compared with adjacent normal tissues. High expression of FAM83A and FAM83A-AS1 predicted worse survival and more advanced clinical stage. Knockdown of FAM83A or FAM83A-AS1 could inhibit the proliferation, migration and invasion of LUAD cells. Moreover, lncRNA FAM83A-AS1 regulated the expression of FAM83A by functioning as competing endogenous RNA for miR-495-3p. These results implicated that FAM83A and FAM83A-AS1 both played oncogenic roles in LUAD and FAM83A-AS1 could regulate the expression of FAM83A by sponging miR-495-3p. The study revealed a novel regulatory mechanism of tumor development in LUAD and FAM83A and FAM83A-AS1 may be novel biomarkers and therapeutic targets for LUAD.

show abstract

“…Recently, overexpression of MTL5 was reported in NSCLC, and its expression was shown to predict prognosis [38]. Another study showed that knockdown of FAM111B induced G 2 /M phase arrest and apoptosis in LUAD cells [39]. These data suggested that miR-143-5p -controlled genes were closely involved in LUAD oncogenesis and molecular pathogenesis.…”

Section: Discussionmentioning

confidence: 99%

Involvement of Dual Strands of miR-143 (miR-143-5p and miR-143-3p) and Their Target Oncogenes in the Molecular Pathogenesis of Lung Adenocarcinoma

Sanada

Seki

Mizuno

et al. 2019

IJMS

View full text Add to dashboard Cite

Our analyses of tumor-suppressive microRNAs (miRNAs) and their target oncogenes have identified novel molecular networks in lung adenocarcinoma (LUAD). Moreover, our recent studies revealed that some passenger strands of miRNAs contribute to cancer cell malignant transformation. Downregulation of both strands of the miR-143 duplex was observed in LUAD clinical specimens. Ectopic expression of these miRNAs suppressed malignant phenotypes in cancer cells, suggesting that these miRNAs have tumor-suppressive activities in LUAD cells. Here, we evaluated miR-143-5p molecular networks in LUAD using genome-wide gene expression and miRNA database analyses. Twenty-two genes were identified as potential miR-143-5p-controlled genes in LUAD cells. Interestingly, the expression of 11 genes (MCM4, RAD51, FAM111B, CLGN, KRT80, GPC1, MTL5, NETO2, FANCA, MTFR1, and TTLL12) was a prognostic factor for the patients with LUAD. Furthermore, knockdown assays using siRNAs showed that downregulation of MCM4 suppressed cell growth, migration, and invasion in LUAD cells. Aberrant expression of MCM4 was confirmed in the clinical specimens of LUAD. Thus, we showed that miR-143-5p and its target genes were involved in the molecular pathogenesis of LUAD. Identification of tumor-suppressive miRNAs and their target oncogenes may be an effective strategy for elucidation of the molecular oncogenic networks of this disease.

show abstract

<p>FAM111B, a direct target of p53, promotes the malignant process of lung adenocarcinoma</p>

Cited by 37 publications

References 27 publications

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

FAM83A and FAM83A‑AS1 both play oncogenic roles in lung adenocarcinoma

Involvement of Dual Strands of miR-143 (miR-143-5p and miR-143-3p) and Their Target Oncogenes in the Molecular Pathogenesis of Lung Adenocarcinoma

Contact Info

Product

Resources

About