YB-1 Protein and Multidrug Resistance of Tumor Cells

Stavrovskaya, A. A.; Stromskaya, Tatyana; Rybalkina, Ekaterina Yu.; Моисеева, Н. И.; Vaiman, A.; Guryanov, Sergey; Ovchinnikov, Lev P.; Генс, Г. П.

doi:10.2174/157436212802481592

Cited by 22 publications

(25 citation statements)

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“…Multiple mechanisms have been hypothesized to play a role in chemotherapeutic drug resistance in cancers and the most important ones are associated with the over-expression of various members of ATP-binding cassette (ABC) MDR1 and MRPs (Gottesman et al, 2002), an increase in detoxification of chemotherapeutic drugs (e.g. glutathione S-transferases: GST) and dihydropyrimidine dehydrogenase: DPD) (Tew, 1994;Nita et al, 1998), as well as an alteration of drug targets and suppression of drug-induced apoptosis (Stavrovskaya, 2000). Several lines of evidence suggest that both MDR1 and MRP1 are the major contributors of the multidrug resistance phenotypes observed in a number of tumor cells (Ambudkar et al, 2003;Larkin et al, 2004).…”

Section: Discussionmentioning

confidence: 99%

Cytotoxicity, Toxicity, and Anticancer Activity of Zingiber Officinale Roscoe Against Cholangiocarcinoma

Plengsuriyakarn¹,

Viyanant²,

Eursitthichai³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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Cholangiocarcinoma (CCA) is an uncommon adenocarcinoma which arises from the epithelial cells of the bile ducts. The aim of the study was to investigate the cytotoxicity, toxicity, and anticancer activity of a crude ethanolic extract of ginger (Zingiber officinale Roscoe) against CCA. Cytotoxic activity against a CCA cell line (CL-6) was assessed by calcein-AM and Hoechst 33342 assays and anti-oxidant activity was evaluated using the DPPH assay. Investigation of apoptotic activity was performed by DNA fragmentation assay and induction of genes that may be involved in the resistance of CCA to anticancer drugs (MDR1, MRP1, MRP2, and MRP3) was examined by real-time PCR. To investigate anti-CCA activity in vivo, a total of 80 OV and nitrosamine (OV/ DMN)-induced CCA hamsters were fed with the ginger extract at doses of 1000, 3000, and 5000 mg/kg body weight daily or every alternate day for 30 days. Control groups consisting of 10 hamsters for each group were fed with 5-fluorouracil (positive control) or distilled water (untreated control). Median IC 50 (concentration that inhibits cell growth by 50%) values for cytotoxicity and anti-oxidant activities of the crude ethanolic extract of ginger were 10.95, 53.15, and 27.86 μg/ml, respectively. More than ten DNA fragments were visualized and up to 7-9 fold up-regulation of MDR1 and MRP3 genes was observed following exposure to the ethanolic extract of ginger. Acute and subacute toxicity tests indicated absence of any significant toxicity at the maximum dose of 5,000 mg/kg body weight given by intragastric gavage. The survival time and survival rate of the CCA-bearing hamsters were significantly prolonged compared to the control group (median of 54 vs 17 weeks). Results from these in vitro and in vivo studies thus indicate promising anticancer activity of the crude ethanolic extract of ginger against CCA with the absence of any significant toxicity. Moreover, MDR1 and MRP3 may be involved in conferring resistance of CCA to the ginger extract.

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Section: Discussionmentioning

confidence: 99%

Cytotoxicity, Toxicity, and Anticancer Activity of Zingiber Officinale Roscoe Against Cholangiocarcinoma

Plengsuriyakarn¹,

Viyanant²,

Eursitthichai³

et al. 2012

Asian Pacific Journal of Cancer Prevention

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“…The most common hypothesis related to Pgp-mediated transport suggests that the drug molecule binds to a specific site of Pgp and one of the ATP-binding domains is activated. Then, the hydrolysis of ATP causes a major change in the shape of Pgp, which causes the release of the drug into the extracellular space (Stavrovskaya, 2000). The MDR family includes two genes in man and only the ABCB1 (also called MDR1/Pgp) gene has been found to cause MDR.…”

Section: Pgp In Anticancer Drug Resistancementioning

confidence: 99%

“…The MDR family includes two genes in man and only the ABCB1 (also called MDR1/Pgp) gene has been found to cause MDR. (Stavrovskaya, 2000). Pgp-related MDR can occur due to alteration of ABCB1 gene expression and amplification of the ABCB1 gene (Borst, 1991).…”

Section: Pgp In Anticancer Drug Resistancementioning

confidence: 99%

“…(Demant et al, 1990) for instance, the acidic environment due to lactic acid production by hypoxic tumor cells has been thought to be responsible for resistance against some drugs whose uptake is dependent on the pH gradient across the membranes (Demant et al, 1990). Cellular resistance mechanisms are defined by alterations in the biochemistry of malignant cells and classified into nonclassical MDR phenotypes and transport-based classical MDR phenotypes (Stavrovskaya, 2000). Non-classical MDR describes non-transport based mechanisms and includes altered activity of enzymes such as glutathione S-transferase (GST) and topoisomerase that can decrease the cytotoxic activity of drugs and changes in the balance of proteins involved in apoptosis (Schisselbauer et al, 1990).…”

Section: Introductionmentioning

confidence: 99%

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Molecular mechanisms of drug resistance and its reversal in cancer

Yandım

Adan-Gokbulut

Baran

2015

Critical Reviews in Biotechnology

280

178

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Chemotherapy is the main strategy for the treatment of cancer. However, the main problem limiting the success of chemotherapy is the development of multidrug resistance. The resistance can be intrinsic or acquired. The resistance phenotype is associated with the tumor cells that gain a cross-resistance to a large range of drugs that are structurally and functionally different. Multidrug resistance arises via many unrelated mechanisms, such as overexpression of energy-dependent efflux proteins, decrease in uptake of the agents, increase or alteration in drug targets, modification of cell cycle checkpoints, inactivation of the agents, compartmentalization of the agents, inhibition of apoptosis and aberrant bioactive sphingolipid metabolism. Exact elucidation of resistance mechanisms and molecular and biochemical approaches to overcome multidrug resistance have been a major goal in cancer research. This review comprises the mechanisms guiding multidrug resistance in cancer chemotherapy and also touches on approaches for reversing the resistance.

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“…Interplay of several protective mechanisms is not uncommon, but one mechanism usually prevails. The best studied mechanisms, whose clinical significance for certain neoplastic forms (such as chronic myeloid leukemia or chronic lymphatic leukemia) has been ascertained, are: activation of transmembrane transport proteins that remove various substances from the cell (namely, Р-glycoproteinPgp); activation of the glutathione system enzymes that detoxify the drugs; modifications in the genes and proteins that control apoptosis and cell survival [51].…”

Section: Caspase Expression In к562 Cells Incubated With 2-meq 2-meqmentioning

confidence: 99%