ArticleBrazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica2014
RNAi-mediated knockdown of FANCF suppresses cell proliferation, migration, invasion, and drug resistance potential of breast cancer cells.
Article in Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologica, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.
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Who cites it
7 citing papers in PubMed, 1 synthesis or guideline pooled it, 14 citations in OpenAlex.
- Hypermethylation of tumor suppressor genes is a risk factor for poor prognosis in ovarian cancer: A meta-analysis.Medicine · 2019Pooled it
- Knockdown of FANCI suppresses hepatocellular carcinoma development via the PI3K/Akt/GSK-3β pathway.Heliyon · 2025Article
- Establishment of prognostic model of bladder cancer based on apoptosis-related genes, in which P4HB promotes BLCA progression.BMC urology · 2023Article
- Genomic comparison between cerebrospinal fluid and primary tumor revealed the genetic events associated with brain metastasis in lung adenocarcinoma.Cell death & disease · 2021Article
- FANCF hypomethylation is associated with colorectal cancer in Han Chinese.The Turkish journal of gastroenterology : the official journal of Turkish Society of Gastroenterology · 2020Article
- FANCI Cooperates with IMPDH2 to Promote Lung Adenocarcinoma Tumor Growth via a MEK/ERK/MMPs Pathway.OncoTargets and therapy · 2020Article
- Overexpression of P16 reversed the MDR1-mediated DDP resistance in the cervical adenocarcinoma by activating the ERK1/2 signaling pathway.Cell division · 2019Article
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Authors and funding
11 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fanconi anemia complementation group F protein (FANCF) is a key factor, which maintains the function of FA/BRCA, a DNA damage response pathway. However, the functional role of FANCF in breast cancer has not been elucidated. We performed a specific FANCF-shRNA knockdown of endogenous FANCF in vitro. Cell viability was measured with a CCK-8 assay. DNA damage was assessed with an alkaline comet assay. Apoptosis, cell cycle, and drug accumulation were measured by flow cytometry. The expression levels of protein were determined by Western blot using specific antibodies. Based on these results, we used cell migration and invasion assays to demonstrate a crucial role for FANCF in those processes. FANCF shRNA effectively inhibited expression of FANCF. We found that proliferation of FANCF knockdown breast cancer cells (MCF-7 and MDA-MB-435S) was significantly inhibited, with cell cycle arrest in the S phase, induction of apoptosis, and DNA fragmentation. Inhibition of FANCF also resulted in decreased cell migration and invasion. In addition, FANCF knockdown enhanced sensitivity to doxorubicin in breast cancer cells. These results suggest that FANCF may be a potential target for molecular, therapeutic intervention in breast cancer.
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