Biochemistry And Microbial Sciences - Research Publications

Permanent URI for this collectionhttps://kr.cup.edu.in/handle/32116/27

Browse

End date: 2020Subject: search.filters.subject.Cancer

Search Results

Now showing 1 - 3 of 3
  • Thumbnail Image
    Item
    Emerging role of ZBTB7A as an oncogenic driver and transcriptional repressor
    (Elsevier, 2020) Gupta, S; Singh, A.K; Prajapati, K.S; Kushwaha, P.P; Shuaib, M; Kumar, S.
    ZBTB7A is a member of the POK family of transcription factors that possesses a POZ-domain at the N-terminus and Krüppel-like zinc-finger at the c-terminus. ZBTB7A was initially isolated as a protein that binds to the inducer of the short transcript of HIV-1 virus TAT gene promoter. The protein forms a homodimer through protein-protein interaction via the N-terminus POZ-domains. ZBTB7A typically binds to the DNA elements through its zinc-finger domains and represses transcription both by modification of the chromatin organization and through the direct recruitment of transcription factors to gene regulatory regions. ZBTB7A is involved in several fundamental biological processes including cell proliferation, differentiation, and development. It also participates in hematopoiesis, adipogenesis, chondrogenesis, cellular metabolism and alternative splicing of BCLXL, DNA repair, development of oligodendrocytes, osteoclast and unfolded protein response. Aberrant ZBTB7A expression promotes oncogenic transformation and tumor progression, but also maintains a tumor suppressive role depending on the type and genetic context of cancer. In this comprehensive review we provide information about the structure, function, targets, and regulators of ZBTB7A and its role as an oncogenic driver and transcriptional repressor in various human diseases. - 2020 Elsevier B.V.
  • No Thumbnail Available
    Item
    Dihydropyrimidine dehydrogenase in the metabolism of the anticancer drugs
    (Springer Verlag, 2019) Sharma V.; Gupta S.K.; Verma M.
    Cancer caused by fundamental defects in cell cycle regulation leads to uncontrolled growth of cells. In spite of the treatment with chemotherapeutic agents of varying nature, multiple resistance mechanisms are identified in cancer cells. Similarly, numerous variations, which decrease the metabolism of chemotherapeutics agents and thereby increasing the toxicity of anticancer drugs have been identified. 5-Fluorouracil (5-FU) is an anticancer drug widely used to treat many cancers in the human body. Its broad targeting range is based upon its capacity to act as a uracil analogue, thereby disrupting RNA and DNA synthesis. Dihydropyrimidine dehydrogenase (DPD) is an enzyme majorly involved in the metabolism of pyrimidines in the human body and has the same metabolising effect on 5-FU, a pyrimidine analogue. Multiple mutations in the DPD gene have been linked to 5-FU toxicity and inadequate dosages. DPD inhibitors have also been used to inhibit excessive degradation of 5-FU for meeting appropriate dosage requirements. This article focusses on the role of dihydropyrimidine dehydrogenase in the metabolism of the anticancer drug 5-FU and other associated drugs.
  • Thumbnail Image
    Item
    Natural Compounds Are Smart Players in Context to Anticancer Potential of Receptor Tyrosine Kinases: An In Silico and In Vitro Advancement
    (Springer, 2017) Singh, Pushpendra; Kumar, Shashank; Bast, Felix
    Cancer is the ruling cause of mortality worldwide. Chemotherapeutic toxicity and drug resistance have provided impulsion for the formulation of new anticancer agents. Receptor tyrosine kinases (RTKs) are the most activated cell surface receptors for copious polypeptide growth factors, cytokines, and hormones that play a considerable role in cancer initiation, promotion, and progression. Natural products are a prime source of new anticancer drugs and their leads. The objective of computer-aided drug design (CADD) is to enhance the set of compounds with prudent active drug-like properties and eliminate inactive, toxic, poor absorption, distribution, metabolism, and excretion toxicity (ADME/T) compounds. In the present chapter, in silico advancement of anticancer natural compounds and molecular mechanisms of action of flavonoids, viz., genistein, myricetin, quercetin, luteolin, morin, kaempferol, catechin, and epigallocatechin gallate (EGCG), on RTK and PI3K signaling pathway attributing to their potential anticancer activity have been discussed.