Insights into a crucial role of TRIP13 in human Cancer

Publication date: Available online 22 June 2019Source: Computational and Structural Biotechnology JournalAuthor(s): S. Lu, J. Qian, M. Guo, C. Gu, Y. YangAbstractThyroid Hormone Receptor Interacting Protein 13 (TRIP13) plays a key role in regulating mitotic processes, including spindle assembly checkpoint and DNA repair pathways, which may account for Chromosome instability (CIN). As CIN is a predominant hallmark of cancer, TRIP13 may act as a tumor susceptibility locus. Amplification of TRIP13 has been observed in various human cancers and implicated in several aspects of malignant transformation, including cancer cell proliferation, drug resistance and tumor progression. Here, we discussed the functional significance of TRIP13 in cell progression, highlighted the recent findings on the aberrant expression in human cancers and emphasized its significance for the therapeutic potential.Graphical Abstract
Source: Computational and Structural Biotechnology Journal - Category: Biotechnology Source Type: research

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Dehydrogenase/reductase SDR family member 2 silencing sensitizes an oxaliplatin‑resistant cell line to oxaliplatin by inhibiting excision repair cross‑complementing group 1 protein expression. Oncol Rep. 2019 Aug 22;: Authors: Li JM, Jiang GM, Zhao L, Yang F, Yuan WQ, Wang H, Luo YQ Abstract Oxaliplatin (Oxa)‑based chemotherapy is widely used as the first‑line treatment for colorectal cancer (CRC). However, Oxa‑resistance is common for many postoperative CRC patients. To explore drug resistance in CRC, an Oxa‑resistant cell line, HCT116/Oxa, was established from parental HCT116 cells. ...
Source: Oncology Reports - Category: Cancer & Oncology Tags: Oncol Rep Source Type: research
Publication date: Available online 22 August 2019Source: Cancer CellAuthor(s): Salma Parvin, Ariel Ramirez-Labrada, Shlomzion Aumann, XiaoQing Lu, Natalia Weich, Gabriel Santiago, Elena M. Cortizas, Eden Sharabi, Yu Zhang, Isidro Sanchez-Garcia, Andrew J. Gentles, Evan Roberts, Daniel Bilbao-Cortes, Francisco Vega, Jennifer R. Chapman, Ramiro E. Verdun, Izidore S. LossosSummaryDeficiency in DNA double-strand break (DSB) repair mechanisms has been widely exploited for the treatment of different malignances, including homologous recombination (HR)-deficient breast and ovarian cancers. Here we demonstrate that diffuse large B...
Source: Cancer Cell - Category: Cancer & Oncology Source Type: research
Publication date: Available online 21 August 2019Source: Journal of Visceral SurgeryAuthor(s): B. Menahem, A. Alves, J.M. Regimbeau, C. SabbaghSummaryNearly 5% of colorectal cancers are related to constitutional genetic abnormalities. In Lynch Syndrome (LS), the abnormality is a mutation of the deoxyribonucleic acid (DNA) repair system. The goal of this update is to update indications and surgical strategies for patients with LS. Different spectra of disease are associated with LS. The narrow spectrum includes cancers with a high relative risk: colorectal cancer (CRC), endometrial cancer, urinary tract cancers and small in...
Source: Journal of Visceral Surgery - Category: Surgery Source Type: research
In this study, we data-mined in silico databases to evaluate aldolase family members’ mRNA expression in glioblastoma patient cohorts for determining its prognostic values. After that, we also performed immunohistochemical stain (IHC) analysis to evaluate protein expression levels of ALDOC in glioblastoma tissues. From The Cancer Genome Atlas (TCGA) database analyses, higher mRNA expression levels in normal brain tissue compared to glioblastoma was observed. In addition, compared to low-grade glioma, ALDOC expression was significantly downregulated in high-grade glioblastoma. Besides, the expression level of ALDO...
Source: Cancers - Category: Cancer & Oncology Authors: Tags: Article Source Type: research
Remarkable advances in understanding breast cancer predisposition have been achieved in the last decade of twentieth century through the identification of two high-penetrance genes, BRCA1 and BRCA2 (1,2). These two genes confer approximately 10-fold increased risk of breast cancer on population with such mutations compared to general population (3). Deleterious mutations in BRCA1 and BRCA2 lead to inactivation of the encoded proteins, consequently failing to induce homologous recombination (HR) to repair the damaged DNA and maintain normal growth of cells.
Source: Cancer Genetics and Cytogenetics - Category: Genetics & Stem Cells Authors: Tags: Original Article Source Type: research
Publication date: Available online 21 August 2019Source: Clinica Chimica ActaAuthor(s): Seyed Mohammad Hosseini, Isobel Okoye, Mitra Ghasemi Chaleshtari, Bita Hazhirkarzar, Javad Mohamadnejad, Gholamreza Azizi, Mohammad Hojjat-Farsangi, Hamed Mohammadi, Siamak Sandoghchian Shotorbani, Farhad Jadidi-NiaraghAbstractDespite the medical advances of the 21st century, the incidence of cancer continues to increase and the search for a universal cure remains a major health challenge. Our lack of understanding the complex pathophysiology of the tumor microenvironment has hindered the development and efficiency of anti-cancer therap...
Source: Clinica Chimica Acta - Category: Laboratory Medicine Source Type: research
Abstract Ataxia telangiectasia mutated (ATM) protein recognizes and repairs DNA double strand breaks (DSB) through activation of cell cycle checkpoints and DNA repair proteins. Atm gene mutations increase female reproductive cancer risk. Phosphoramide mustard (PM) induces ovarian DNA damage and destroys primordial follicles, and pharmacological ATM inhibition prevents PM-induced follicular depletion. Wild-type (WT) C57BL/6 or Atm+/- mice were dosed once intraperitoneally with sesame oil (95%) or PM (25 mg/kg) in the proestrus phase of the estrous cycle and ovaries harvested 3 days thereafter. Atm+/- mice...
Source: Biology of Reproduction - Category: Reproduction Medicine Authors: Tags: Biol Reprod Source Type: research
Factor XII (FXII) is the zymogen of serine protease, factor XIIa (FXIIa). FXIIa enzymatic activities have been extensively studied and FXIIa inhibition is emerging as a promising target to treat or prevent thrombosis without creating a hemostatic defect. FXII and plasma prekallikrein reciprocally activate each other and result in liberation of bradykinin. Due to its unique structure among coagulation factors, FXII exerts mitogenic activity in endothelial and smooth muscle cells, indicating that zymogen FXII has activities independent of its protease function. A growing body of evidence has revealed that both FXII and FXIIa...
Source: Frontiers in Immunology - Category: Allergy & Immunology Source Type: research
Here, we report that Sam68, an early signaling molecule in DDR, is elevated in skin tumor tissues derived from NMSC patients and skin lesions from Gli2 ‐transgenic mice. Downregulation of Sam68 impacts the growth and survival of human tumor keratinocytes and genetic ablation of Sam68 delays the onset of basal cell carcinomas (BCC) in Gli2‐transgenic mice. Moreover, Sam68 plays a critical role in DNA damage‐induced DNA repair and nuclear facto r kappa B (NF‐κB) signaling pathways in keratinocytes, hence conferring keratinocyte sensitivity to DNA damaging agents. AbstractAlthough targeting DNA repair signaling ...
Source: Cancer Medicine - Category: Cancer & Oncology Authors: Tags: ORIGINAL RESEARCH Source Type: research
Authors: Cheah PL, Li J, Looi LM, Koh CC, Lau TP, Chang SW, Teoh KH, Mun KS, Nazarina AR Abstract Since 2014, the National Comprehensive Cancer Network (NCCN) has recommended that colorectal carcinoma (CRC) be universally tested for high microsatellite instability (MSI-H) which is present in 15% of such cancers. Fidelity of resultant microsatellites during DNA replication is contingent upon an intact mismatch repair (MMR) system and lack of fidelity can result in tumourigenesis. Prior to commencing routine screening for MSI-H, we assessed two commonly used methods, immunohistochemical (IHC) determination of loss of...
Source: Malaysian Journal of Pathology - Category: Pathology Tags: Malays J Pathol Source Type: research
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