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Official Full Name
BRCA1 interacting protein C-terminal helicase 1
Fanconi anemia group J protein is a protein that in humans is encoded by the BRCA1-interacting protein 1 (BRIP1) gene. The protein encoded by this gene is a member of the RecQ DEAH helicase family and interacts with the BRCT repeats of breast cancer, type 1 (BRCA1). The bound complex is important in the normal double-strand break repair function of breast cancer, type 1 (BRCA1). This gene may be a target of germline cancer-inducing mutations. This protein also appears to be important in ovarian cancer where it seems to act as an antioncogene
BRIP1; BRCA1 interacting protein C-terminal helicase 1; OF; BACH1; FANCJ; Fanconi anemia group J protein; ATP-dependent RNA helicase BRIP1; BRCA1/BRCA2-associated helicase 1; BRCA1-associated C-terminal helicase 1; BRCA1-binding helicase-like protein; BRCA1-interacting protein C-terminal helicase 1; FLJ90232; MGC126521; MGC126523; BRCA1-interacting protein 1; BRCA1/BRCA2 associated helicase 1; BRCA1-binding helicase-like protein BACH1; Fanconi anemia group J protein homolog; si:ch211-158l18.1; Fanconi anemia J; complementation group J

BRCA1 interacting protein 1 (BRIP1), which cooperates with many DNA metabolic proteins involved in DNA damage detection and repair, and plays an important role in cell cycle checkpoint control. BRIP1 is a DNA-dependent ATPase and a 5'-3' DNA helicase, which achieves its cancer suppression function and DNA double-strand break repair through direct interaction with a highly conserved C-terminal BRCT (BRCA1 C-terminal domain) protein domain repeats of the tumor suppressor BRCA1. The N-terminal 888-residue structure of BRIP1 shows strong homology to the catalytic and nucleotide binding domains of the DEAH helicase family members. Abnormal BRIP1 function contributes to tumor induction. In fact, BRCA1 repeats mutations within BRCT1 disrupting its interaction with BRIP1 and leading to DNA repair defects leading to multiple forms of cancer.

BRIP1 and cervical cancer

Cervical cancer is the second most common cancer among women worldwide and is an important cause of morbidity and mortality rate. Liu et al. constructed a BRIP1 recombinant plasmid that was overexpressed in the cervical cancer cell line (HeLa) and found that ectopic expression of BRIP1 significantly enhanced the antitumor activity of cisplatin. In addition, BRIP1 promoted cisplatin-mediated apoptosis and inhibited tumor angiogenesis. Synergistic inhibition of BRIP1 has been reported to be partially due to attenuated Rac1 GTPase activation, and Rac1 GTPase reactivation could reverse BRIP1-induced sensitization. In conclusion, up-regulation of BRIP1 can enhance the chemosensitivity of HeLa cells to cisplatin by inhibiting the activation of Rac1 GTPase, providing new insights into the important role of BRIP1 in cervical cancer chemotherapy.


Hepatocellular carcinoma (HCC) is the most common primary malignancy in the liver. The BRIP1 locus is closely associated with HCC risk in patients with HBV- and/or HCV-induced liver disease, even after adjusting for age, sex, body mass index, alcohol consumption, aminotransferase levels, disease duration, viral cirrhosis etiology, and potential population admixture. The current research results show investigating in experimental models the BRIP1 phosphorylation pathway and its interaction with BLM as a possible mechanisms of liver carcinogenesis. Previous preclinical studies have shown that PARP inhibition is a potentially promising HCC treatment strategy. Recent studies have revealed that BRIP1 genotyping should be used to predict the efficacy of forthcoming trials of HCC treatments that will target this pathway.


The incidence of global head and neck squamous cell carcinoma (SCCHN) has increased significantly in the last 10 years, especially in women. Recently, the study found that single nucleotide polymorphisms (SNPs) rs7213430 in BRIP1 was significantly associated with SCCHN risk. In addition, functional analysis revealed that SNP rs7213430 is in the miR-101 seed binding region, and variant G alleles could result in significantly lower luciferase activity and BRIP1 mRNA expression, compared to the A allele with the presence of miR-101. The current results indicate that SNP rs7213430 in the 3'-UTR of BRIP1 might cause SCCHN susceptibility by affecting the binding activity of miR-101 and lead to a decrease in BRIP1 expression.

In conclusion, BRIP1 is required for BRCA-associated DNA damage repair function and may be involved in tumorigenesis and invasiveness of various cancers. Therefore, further study of the function of BRIP1 and its mechanism of action in cancer will provide new insights into the treatment of related diseases.


  1. Abderrahim O, et al. BRIP1 coding variants are associated with a high risk of hepatocellular carcinoma occurrence in patients with HCV- or HBV-related liver disease. Oncotarget, 2017, 8(38): 62842-62857
  2. Wei Z, et al. BRIP1 inhibits the tumorigenic properties of cervical cancer by regulating RhoA GTPase activity. Oncology Letters, 2016, 11: 551-558
  3. Liu HL, et al. A variant at a potentially functional microRNA-binding site in BRIP1 was associated with risk of squamous cell carcinoma of the head and neck. Tumour Biol, 2016, 37(6): 8057–8066
  4. Ishita Gupta, et al. BRIP1 overexpression is correlated with clinical features and survival outcome of luminal breast cancer subtypes. Endocrine Connections, 2018, 7: 65–77

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