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Article ; Online: Can Nitric Oxide-Based Therapy Be Improved for the Treatment of Cancers? A Perspective.

Sinha, Birandra K

International journal of molecular sciences

2023 Volume 24, Issue 17

Abstract: Since the early observations that nitric oxide ( ...

Abstract	Since the early observations that nitric oxide (
MeSH term(s)	Humans ; Nitric Oxide ; Prospective Studies ; Neoplasms/drug therapy ; ATP-Binding Cassette Transporters ; Polymers
Chemical Substances	Nitric Oxide (31C4KY9ESH) ; ATP-Binding Cassette Transporters ; Polymers
Language	English
Publishing date	2023-09-02
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms241713611
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Article: A Role for iNOS in Erastin Mediated Reduction of P-Glycoprotein Transport Activity.

Brown, Shalyn M / Sinha, Birandra K / Cannon, Ronald E

Cancers

2024 Volume 16, Issue 9

Abstract: The blood-brain barrier is composed of both a physical barrier and an enzymatic barrier. Tight junction (TJ) proteins expressed between endothelial cells of brain capillaries provide the physical barrier to paracellular movement of ions and molecules to ... ...

Abstract	The blood-brain barrier is composed of both a physical barrier and an enzymatic barrier. Tight junction (TJ) proteins expressed between endothelial cells of brain capillaries provide the physical barrier to paracellular movement of ions and molecules to the brain, while luminal-facing efflux transporters enzymatically restrict the entry of blood-borne molecules from entering the brain. The expression and activity of ATP Binding Cassette transporters or "ABC" transporters in endothelial cells of the BBB and in human tumor cells are dynamically regulated by numerous signaling pathways. P-glycoprotein (P-gp), (ABCB1), is arguably the most studied transporter of the BBB, and in human cell lines. P-glycoprotein transport activity is rapidly inhibited by signaling pathways that call for the rapid production of nitric oxide (NO) from the inducible nitric oxide synthase enzyme, iNOS. This study investigated how nano-molar levels of the selective chemotherapeutic erastin affect the activity or expression of P-glycoprotein transporter in brain capillaries and in human tumor cell lines. We chose erastin because it signals to iNOS for NO production at low concentrations. Furthermore, erastin inhibits the cellular uptake of cystine through the X
Language	English
Publishing date	2024-04-29
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers16091733
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Article ; Online: Molecular Mechanisms of Cytotoxicity of NCX4040, the Non-Steroidal Anti-Inflammatory NO-Donor, in Human Ovarian Cancer Cells.

Sinha, Birandra K / Tokar, Erik J / Bortner, Carl D

International journal of molecular sciences

2022 Volume 23, Issue 15

Abstract: NCX4040, the non-steroidal anti-inflammatory-NO donor, is cytotoxic to several human tumors, including ovarian tumor cells. We have found that NCX4040 is also cytotoxic against both OVCAR-8 and its adriamycin resistant (NCI/ADR-RES) tumor cell lines. ... ...

Abstract	NCX4040, the non-steroidal anti-inflammatory-NO donor, is cytotoxic to several human tumors, including ovarian tumor cells. We have found that NCX4040 is also cytotoxic against both OVCAR-8 and its adriamycin resistant (NCI/ADR-RES) tumor cell lines. Here, we have examined mechanism(s) for the cytotoxicity of NCX4040 in OVCAR-8 and NCI/ADR-RES cell lines. We found that NCX4040 induced significant apoptosis in both cell lines. Furthermore, NCX4040 treatment caused significant depletion of cellular glutathione, causing oxidative stress due to the formation of reactive oxygen/nitrogen species (ROS/RNS). Significantly more ROS/RNS were detected in OVCAR-8 cells than in NCI/ADR-RES cells which may have resulted from increased activities of SOD, glutathione peroxidase and transferases expressed in NCI/ADR-RES cells. NCX4040 treatment resulted in the formation of double-strand DNA breaks in both cells; however, more of these DNA breaks were detected in OVCAR-8 cells. RT-PCR studies indicated that NCX4040-induced DNA damage was not repaired as efficiently in NCI/ADR-RES cells as in OVCAR-8 cells which may lead to a differential cell death. Pretreatment of OVCAR-8 cells with N-acetylcysteine (NAC) significantly decreased cytotoxicity of NCX4040 in OVCAR-8 cells; however, NAC had no effects on NCX4040 cytotoxicity in NCI/ADR-RES cells. In contrast, FeTPPS, a peroxynitrite scavenger, completely blocked NCX4040-induced cell death in both cells, suggesting that NCX4040-induced cell death could be mediated by peroxynitrite formed from NCX4040 following cellular metabolism.
MeSH term(s)	Anti-Inflammatory Agents, Non-Steroidal/therapeutic use ; Antineoplastic Agents/pharmacology ; Aspirin/analogs & derivatives ; Carcinoma, Ovarian Epithelial ; Doxorubicin/pharmacology ; Female ; Humans ; Nitro Compounds ; Ovarian Neoplasms/pathology ; Peroxynitrous Acid ; Reactive Nitrogen Species ; Reactive Oxygen Species
Chemical Substances	Anti-Inflammatory Agents, Non-Steroidal ; Antineoplastic Agents ; NCX 4040 ; Nitro Compounds ; Reactive Nitrogen Species ; Reactive Oxygen Species ; Peroxynitrous Acid (14691-52-2) ; Doxorubicin (80168379AG) ; Aspirin (R16CO5Y76E)
Language	English
Publishing date	2022-08-03
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2019364-6
ISSN	1422-0067 ; 1422-0067 ; 1661-6596
ISSN (online)	1422-0067
ISSN	1422-0067 ; 1661-6596
DOI	10.3390/ijms23158611
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Article: Nitric oxide: Friend or Foe in Cancer Chemotherapy and Drug Resistance: A Perspective.

Sinha, Birandra K

Journal of cancer science & therapy

2016 Volume 8, Page(s) 244–251

Abstract: A successful treatment of cancers in the clinic has been difficult to achieve because of the emergence of drug resistant tumor cells. While various approaches have been tried to overcome multi-drug resistance, it has remained a major road block in ... ...

Abstract	A successful treatment of cancers in the clinic has been difficult to achieve because of the emergence of drug resistant tumor cells. While various approaches have been tried to overcome multi-drug resistance, it has remained a major road block in achieving complete success in the clinic. Extensive research has identified various mechanisms, including overexpression of P-glycoprotein 170, modifications in activating or detoxification enzymes (phase I and II enzymes), and mutation and/or decreases in target enzymes in cancer cells. However, nitric oxide and/or nitric oxide-related species have not been considered an important player in cancer treatment and or drug resistance. Here, we examine the significance of nitric oxide in the treatment and resistance mechanisms of various anticancer drugs. Furthermore, we describe the significance of recently reported effects of nitric oxide on topoisomerases and the development of resistance to topoisomerase-poisons in tumor cells.
Language	English
Publishing date	2016-10-28
Publishing country	United States
Document type	Journal Article
ZDB-ID	2578254-X
ISSN	1948-5956
ISSN	1948-5956
DOI	10.4172/1948-5956.1000421
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Article: NCX-4040, a Unique Nitric Oxide Donor, Induces Reversal of Drug-Resistance in Both ABCB1- and ABCG2-Expressing Multidrug Human Cancer Cells.

Sinha, Birandra K / Perera, Lalith / Cannon, Ronald E

Cancers

2021 Volume 13, Issue 7

Abstract: The emergence of multidrug resistance (MDR) in the clinic is a significant problem for a successful treatment of human cancers. Overexpression of various ABC transporters (P-gp, BCRP and MRP's), which remove anticancer drugs in an ATP-dependent manner, ... ...

Abstract	The emergence of multidrug resistance (MDR) in the clinic is a significant problem for a successful treatment of human cancers. Overexpression of various ABC transporters (P-gp, BCRP and MRP's), which remove anticancer drugs in an ATP-dependent manner, is linked to the emergence of MDR. Attempts to modulate MDR have not been very successful in the clinic. Furthermore, no single agent has been found to significantly inhibit their functions to overcome clinical drug resistance. We have previously shown that nitric oxide (
Language	English
Publishing date	2021-04-02
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2527080-1
ISSN	2072-6694
ISSN	2072-6694
DOI	10.3390/cancers13071680
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Article: Elucidation of Mechanisms of Topotecan-Induced Cell Death in Human Breast MCF-7 Cancer Cells by Gene Expression Analysis.

Sinha, Birandra K / Tokar, Erik J / Bushel, Pierre R

Frontiers in genetics

2020 Volume 11, Page(s) 775

Abstract: Topotecan is a clinically active anticancer agent for the management of various human tumors. While the principal mechanism of tumor cell killing by topotecan is due to its interactions with topoisomerase I and formation of DNA double-strand breaks, ... ...

Abstract	Topotecan is a clinically active anticancer agent for the management of various human tumors. While the principal mechanism of tumor cell killing by topotecan is due to its interactions with topoisomerase I and formation of DNA double-strand breaks, recent studies suggest that mechanisms involving generation of reactive free radicals and induction of oxidative stress may play a significant role in topotecan-dependent tumor cell death. We have shown that topotecan generates a topotecan radical following one-electron oxidation by a peroxidase-hydrogen peroxide system which reacts with reduced glutathione and cysteine, forming the glutathiyl and cysteinyl radicals, respectively. While little is known how these events are involved in topotecan-induced tumor cell death, we have now examined the effects of topotecan short (1 h) and long (24 h) exposure on global gene expression patterns using gene expression microarray analysis in human breast MCF-7 cancer cells, a wild-type p53 containing cell line. We show here that topotecan treatment significantly down-regulated estrogen receptor alpha (ERα/ESR1) and antiapoptotic BCL2 genes in addition to many other p53-regulated genes. Furthermore, 8-oxoguanine DNA glycosylase (OGG1), ferredoxin reductase (FDXR), methionine sulfoxide reductase (MSR), glutathione peroxidases (GPx), and glutathione reductase (GSR) genes were also differentially expressed by topotecan treatment. The differential expression of these genes was observed in a wild-type p53-containing breast ZR-75-1 tumor cell line following topotecan treatment. The involvement of reactive oxygen free radical sensor genes, the oxidative DNA damage (OGG1) repair gene and induction of pro-apoptotic genes suggest that reactive free radical species play a role in topotecan-induced tumor cell death.
Language	English
Publishing date	2020-07-17
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606823-0
ISSN	1664-8021
ISSN	1664-8021
DOI	10.3389/fgene.2020.00775
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Article ; Online: Ferroptosis-Mediated Cell Death Induced by NCX4040, The Non-Steroidal Nitric Oxide Donor, in Human Colorectal Cancer Cells: Implications in Therapy.

Sinha, Birandra K / Bortner, Carl D / Jarmusch, Alan K / Tokar, Erik J / Murphy, Carri / Wu, Xian / Winter, Heather / Cannon, Ronald E

Cells

2023 Volume 12, Issue 12

Abstract: Our recent studies show that the treatment of human ovarian tumor cells with NCX4040 results in significant depletions of cellular glutathione, the formation of reactive oxygen/nitrogen species and cell death. NCX4040 is also cytotoxic to several human ... ...

Abstract	Our recent studies show that the treatment of human ovarian tumor cells with NCX4040 results in significant depletions of cellular glutathione, the formation of reactive oxygen/nitrogen species and cell death. NCX4040 is also cytotoxic to several human colorectal cancer (CRC) cells in vitro and in vivo. Here, we examined the ferroptosis-dependent mechanism(s) of cytotoxicity of NCX4040 in HT-29 and K-RAS mutant HCT 116 colon cell lines. Ferroptosis is characterized by the accumulation of reactive oxygen species (ROS) within the cell, leading to an iron-dependent oxidative stress-mediated cell death. However, its relevance in the mechanism of NCX4040 cytotoxicity in CRCs is not known. We found that NCX4040 generates ROS in CRC cells without any depletion of cellular GSH. Combinations of NCX4040 with erastin (ER) or RSL3 (RAS-selective lethal 3), known inducers of ferroptosis, enhanced CRC death. In contrast, ferrostatin-1, an inhibitor of ferroptosis, significantly inhibited NCX4040-induced cell death. Treatment of CRC cells with NCX4040 resulted in the induction of lipid peroxidation in a dose- and time-dependent manner. NCX4040 treatment induced several genes related to ferroptosis (e.g., CHAC1, GPX4 and NOX4) in both cell lines. Metabolomic studies also indicated significant increases in both lipid and energy metabolism following the drug treatment in HT-29 and HCT 116 cells. These observations strongly suggest that NCX4040 causes the ferroptosis-mediated cell death of CRC cells. Furthermore, combinations of NCX4040 and ER or RSL3 may contribute significantly to the treatment of CRC, including those that are difficult to treat due to the presence of Ras mutations in the clinic. NCX4040-induced ferroptosis may also be a dynamic form of cell death for the treatment of other cancers.
MeSH term(s)	Humans ; Nitric Oxide Donors/pharmacology ; Ferroptosis ; Reactive Oxygen Species/metabolism ; Carbolines/pharmacology ; Cell Death ; Glutathione/metabolism ; Colorectal Neoplasms/drug therapy
Chemical Substances	NCX 4040 ; Nitric Oxide Donors ; Reactive Oxygen Species ; Carbolines ; Glutathione (GAN16C9B8O)
Language	English
Publishing date	2023-06-14
Publishing country	Switzerland
Document type	Journal Article ; Research Support, N.I.H., Intramural
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells12121626
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Article ; Online: Reversal of drug resistance by JS-K and nitric oxide in ABCB1- and ABCG2-expressing multi-drug resistant human tumor cells.

Sinha, Birandra K / Perera, Lalith / Cannon, Ronald E

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie

2019 Volume 120, Page(s) 109468

Abstract: Development of resistance to chemotherapy drugs is a significant problem in treating human malignancies in the clinic. Overexpression of ABC transporter proteins, including P-170 glycoprotein (P-gp), and breast cancer resistance protein (BCRP, ABCG2) ... ...

Abstract	Development of resistance to chemotherapy drugs is a significant problem in treating human malignancies in the clinic. Overexpression of ABC transporter proteins, including P-170 glycoprotein (P-gp), and breast cancer resistance protein (BCRP, ABCG2) have been implicated in this multi-drug resistance (MDR). These ABC transporters are ATP-dependent efflux proteins. We have recently shown that nitric oxide (NO) inhibits the ATPase activities of P-gp, resulting in a significant enhancement of drug accumulation and the reversal of multi-drug resistance in NCI/ADR-RES cells, a P-gp-overexpressing human MDR cell line. In this study, we used [O
MeSH term(s)	ATP Binding Cassette Transporter, Subfamily B, Member 1 ; ATP Binding Cassette Transporter, Subfamily G, Member 2 ; ATP-Binding Cassette Transporters/antagonists & inhibitors ; Azo Compounds/chemistry ; Azo Compounds/pharmacology ; Cell Line, Tumor ; Cell Survival ; Dose-Response Relationship, Drug ; Doxorubicin/pharmacology ; Drug Resistance, Multiple/drug effects ; Drug Resistance, Neoplasm/drug effects ; Humans ; Mitoxantrone/chemistry ; Mitoxantrone/pharmacology ; Molecular Docking Simulation ; Molecular Structure ; Nitric Oxide/pharmacology ; Nitroso Compounds/chemistry ; Nitroso Compounds/pharmacology ; Piperazines/chemistry ; Piperazines/pharmacology ; Topotecan/chemistry ; Topotecan/pharmacology
Chemical Substances	ATP Binding Cassette Transporter, Subfamily B, Member 1 ; ATP Binding Cassette Transporter, Subfamily G, Member 2 ; ATP-Binding Cassette Transporters ; Azo Compounds ; Nitroso Compounds ; O(2)-(2,4-dinitrophenyl) 1-((4-ethoxycarbonyl)piperazin-1-yl)diazen-1-ium-1,2-diolate ; Piperazines ; 2,2'-(hydroxynitrosohydrazono)bis-ethanamine (146724-94-9) ; Nitric Oxide (31C4KY9ESH) ; Topotecan (7M7YKX2N15) ; Doxorubicin (80168379AG) ; Mitoxantrone (BZ114NVM5P)
Language	English
Publishing date	2019-10-09
Publishing country	France
Document type	Journal Article
ZDB-ID	392415-4
ISSN	1950-6007 ; 0753-3322 ; 0300-0893
ISSN (online)	1950-6007
ISSN	0753-3322 ; 0300-0893
DOI	10.1016/j.biopha.2019.109468
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Article: IS METABOLIC ACTIVATION OF TOPOISOMERASE II POISONS IMPORTANT IN THE MECHANISM OF CYTOTOXICITY?

Sinha, Birandra K / Mason, Ronald P

Journal of drug metabolism & toxicology

2015 Volume 6, Issue 3

Abstract: The antitumor drugs doxorubicin and etoposide, a phodophyllotoxin derivative, are clinically active for the treatment of human malignancies. Because of their extreme effectiveness in the clinic, their modes of actions have been the subject of intense ... ...

Abstract	The antitumor drugs doxorubicin and etoposide, a phodophyllotoxin derivative, are clinically active for the treatment of human malignancies. Because of their extreme effectiveness in the clinic, their modes of actions have been the subject of intense research for over several decades both in the laboratory and in the clinic. It has been found that both doxorubicin and etoposide (VP-16) act on topoisomerase II, induce DNA cleavage, and form double-strand breaks, causing tumor cell death. However, both of these drugs also undergo extensive metabolism in tumor cells and
Language	English
Publishing date	2015-07-24
Publishing country	United States
Document type	Journal Article
ISSN	2157-7609
ISSN	2157-7609
DOI	10.4172/2157-7609.1000186
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Article: BIOTRANSFORMATION OF HYDRAZINE DERVATIVES IN THE MECHANISM OF TOXICITY.

Sinha, Birandra K / Mason, Ronald P

Journal of drug metabolism & toxicology

2014 Volume 5, Issue 3

Abstract: Hydrazine derivatives are environmental and food pollutants but are also important because of their use in medicine for the treatment of tuberculosis and cancer. However, hydrazines also pose significant health risks to humans as they are mutagenic and ... ...

Abstract	Hydrazine derivatives are environmental and food pollutants but are also important because of their use in medicine for the treatment of tuberculosis and cancer. However, hydrazines also pose significant health risks to humans as they are mutagenic and carcinogenic. This review examines various metabolic pathways (enzymatic and non-enzymatic) of hydrazines for the formation of reactive species that bind to cellular macromolecules and lead to cellular dysfunction. It is believed that this biotransformation is responsible for the pharmacology and pathophysiology of hydrazine derivatives.
Language	English
Publishing date	2014-07-08
Publishing country	United States
Document type	Journal Article
ISSN	2157-7609
ISSN	2157-7609
DOI	10.4172/2157-7609.1000168
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