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کاربرد نوع شرط:
- جایگاه : پژوهشی
- مجله: Asian Pacific Journal of Cancer Prevention
- نوع مقاله: Journal Article
- کلمات کلیدی: cancer,Molecular docking,DNA damage,NNK,NNAL
- چکیده:
- چکیده انگلیسی: Purpose: DNA damage is a continuous process occurring within the cells caused by intrinsic and extrinsic factors, but it gets repaired regularly. If the DNA repair process is faulty, the incidences of damages/mutations can accumulate in cells resulting in cell transformation. It is hypothesized that the negative variations in DNA repair pathways in even at one point viz. genetic, translational or posttranslational stage may fairly be crucial for the beginning and development of carcinogenesis. Therefore, we investigated the potential of tobacco specific nitrosamines (TSNs) related carcinogens to interact with the enzymes involved in DNA repair mechanisms in the current study. Methods: The derivatives of cigarettes’ smoke like NNK and NNAL are very well known and recognized carcinogens. Therefore, almost 120 enzymes playing crucial role in the DNA repair process have been analysed for their reactivity with NNK and NNAL. Results: The molecular docking study helped to screen out, 07 possible DNA repair enzyme targets for NNK, and 12for NNAL. Present study revealed the loss of activity of DNA repair enzymes in the presence of NNK and NNAL, and this accumulation may induce the tendency of DNA damage which can lead the transformation of exposed normal cells in to cancerous cells. This study also demonstrated the protective potential of nanoparticles like SWCNTs/MWCNTs against TSN’s induced toxicity; here SWCNT against NNK (-17.16 Kcal/Mol) and MWCNT against NNK -17.01 Kcal/Mol were showing maximum binding affinities than the known biomolecular target of NNK 1UGH (Uracil-DNA glycosylase,-7.82Kcal/Mol). Conclusion: CNTs can be applied as chemo-preventive agents against environmental and tobacco induced carcinogens owing to their scavenging potential and warrants for in vivo and in vitro experimental validation of the results obtained from the present study.
- انتشار مقاله: 05-04-1399
- نویسندگان: Anukriti Dhasmana,Anupam Dhasmana,Hobani Yahya H,Abdullah Farasani,Mahmoud Habibullah,Freah L Alshammary,Saif Khan,Shafiul Haque,Mohtashim Lohani
- مشاهده
- جایگاه : پژوهشی
- مجله: Asian Pacific Journal of Cancer Prevention
- نوع مقاله: Journal Article
- کلمات کلیدی: Breast cancer,Polymorphism,Vitamin D,Vitamin D receptor,Fok1
- چکیده:
- چکیده انگلیسی: Breast cancer is the leading cause of death among women worldwide. It is a multi-factorial disease caused by
genetic and environmental factors. Vitamin D has been hypothesized to lower the risk of breast cancer via the nuclear
vitamin D receptor (VDR). Genetic variants of these vitamin D metabolizing genes may alter the bioavailability of
vitamin D, and hence modulate the risk of breast cancer. Materials and Methods: The distribution of Fok1 VDR gene
(rs2228570) polymorphism and its association with breast cancer was analysed in a case–control study based on 125
breast cancer patients and 125 healthy females from North Indian population, using PCR-RFLP. An In silico exploration
of the probable mechanism of increased risk of breast cancer was performed to investigate the role of single nucleotide
polymorphisms (SNPs) in cancer susceptibility. Results: The Fok1 ff genotype was significantly associated with an
increased risk of breast cancer (p=0.001; χ2=13.09; OR=16.909; %95 CI=2.20 - 130.11). In silico analysis indicated
that SNPs may lead to a loss in affinity of VDR to calcitriol, and may also cause the impairment of normal interaction
of liganded VDR with its heterodimeric partner, the retinoid X receptor (RXR), at protein level, thereby affecting target
gene transcription. Conclusion: Breast cancer risk and pathogenesis in females can be influenced by SNPs. SNPs in
VDR may cause alterations in the major molecular actions of VDR, namely ligand binding, heterodimerization and
transactivation. VDRE binding and co-activator recruitment by VDR appear to be functionally inseparable events that
affect vitamin D-elicited gene transcription. This indicates that breast cancer risk and pathogenesis in females may be
influenced by SNPs.- انتشار مقاله: 04-05-1397
- نویسندگان: Sana Raza,Anupam Dhasmana,Madan Lal Brahma Bhatt,Mohtashim Lohani,Jamal M Arif
- مشاهده