In addition, NO has other multiple synergistic cancer treatment functions, including tumor tissue vasodilatation for drug extravasation promotion, P-glycoprotein (P-gp) downregulation for drug efflux inhibition, and glutathione depletion for cancer cell endogenous antioxidant defense destruction.
Overexpression of ATP-binding cassette subfamily B member 1 (ABCB1)-encoded multidrug resistance protein 1 (MDR1) constitutes a major mechanism of cancer drug resistance including docetaxel (DTX) and cabazitaxel (CTX) resistance in castration-resistant prostate cancer (CRPC).
Overexpression of ATP-binding cassette (ABC) transporters, such as ABCB1 and ABCG2, has been proved to be a major trigger for multidrug resistance (MDR) in certain types of cancer.
The link between bacterial and viral infections to cancer compels us to highlight fascinating reports from coumarin isolation from microorganisms; comment on the recent bioavailability studies of natural or derived coumarins; and discuss our perspectives with respect to bioisosterism in coumarins, p-glycoprotein inhibition and covalent modification, and bioprobes.
Multidrug resistance to anticancer drugs, which is often associated with enhanced expression of the ATP‑binding cassette (ABC) transporter P‑glycoprotein (encoded by the ABCB1 gene) may limit the effects of cancer therapy.
Although nanodrugs have been shown to evade P-glycoprotein (P-gp) recognition and reverse multi-drug resistance (MDR) in cancer, a specific mechanism of how nanodrugs reverse MDR is still unclear.
Multidrug resistance (MDR) in cancer cells is often associated with overexpression of ATP-binding cassette (ABC) transporters, including P-glycoprotein (P-gp/ABCB1), multidrug resistance-associated protein 1 (MRP1/ABCC1) and breast cancer resistance protein (BCRP/ABCG2).
The aim of this study was to evaluate the association between OPRM1 and ABCB1 polymorphisms on pain relief with epidural sufentanil in 69 patients after rectosigma resection for cancer.
In this study, we demonstrated that EBV latent infection induced intracellular ROS production and increased ROS levels triggered elevated P-gp expression, which resulted in strong resistance to existing anti-cancer drugs in EBV-positive lymphoma cell lines and in patients' tissue samples.
Resistance to chemotherapeutic drugs in cancer cells is frequently associated with high expression of p-glycoprotein, a transporter in the plasma membrane that can mediate cellular drug export.
Furthermore, multidrug resistance protein 1 (MDR1) expression in k562/dox cells was downregulated by levistolide A in a dose‑dependent manner, thus suggesting that levistolide A may modulate MDR1 during cancer therapy.
The ATP-binding cassette transporter G2 (ABCG2; also known as breast cancer resistance protein, BCRP) has been suggested to be involved in clinical multidrug resistance (MDR) in cancer like other ABC transporters such as ABCB1 (<i>P</i>-glycoprotein).
Sulfocoumarins, specific carbonic anhydrase IX and XII inhibitors, interact with cancer multidrug resistant phenotype through pH regulation and reverse P-glycoprotein mediated resistance.
Among these exporters, P-glycoprotein and MRP1 are involved in cancer multidrug resistance, protection from endo and xenobiotics, determination of drug pharmacokinetics, and the pathophysiology of a variety of disorders.
One of the most widely used drugs, doxorubicin (Dox) is a substrate of three different ATP-binding cassette (ABC) transporters, namely, ABCB1, ABCG2 and ABCC1, predominantly contributing to MDR phenotype in cancer.
The present study demonstrated that ZA-A, ZA-B and ZA-C, popular triterpenoids from T. camphoratus, effectively modulated the drug efflux transporter P-gp and reversed the cancer MDR issue.
Multidrug resistance is a major cause of failure in the clinical cancer therapy, in which the overexpression of P-glycoprotein (P-gp) plays a crucial role.
P-glycoprotein (P-gp) is a multidrug transporter, which harnesses the chemical energy of ATP to power the efflux of diverse chemotherapeutics out of cells and thus contributes to the development of multidrug resistance (MDR) in cancer.
Out of the eleven screened potent inhibitors, compound (8) exhibited the excellent bioavailability radar against the six molecular descriptors, good absorption, distribution, metabolism and excretion properties along with P-glycoprotein, CYP450 isozymes and membranes permeability profile, on the basis of these factual observations compound (8) can be predict to get in-vivio experimental clearance efficiently, Therefore in future it can be a drug in market, to treat the various disorders associated with the over expression of β-Glucuronidase, enzyme including various types of cancers, particularly hormone-dependent cancers such as (breast, prostate, and colon cancer), while other compounds (1-7, & 9-11), are also showing good predictive pharmacokinetics, medicinal chemistry , BBB and HIA membranes permeability profiles with the requirement of slight lead optimization to get the improved and enhance results.