Ectonucleoside triphosphate diphosphohydrolase 6 expression in testis and testicular cancer and its implication in cisplatin resistance

Tada, Yasuhiro; Yokomizo, Akira; Shiota, Masaki; Song, Yu; Kashiwagi, Eiji; Kuroiwa, Kentaro; Oda, Yoshinao; Naito, Seiji

doi:10.3892/or.2011.1274

Cited by 10 publications

(8 citation statements)

References 19 publications

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“…Cisplatin is one of most commonly used chemotherapeutic drugs in the treatment of solid tumors including liver [1], lung [2], breast [3], cervical [4], ovarian [5], and testis [6] cancers. Although cisplatin has been shown to be one of the most effective anticancer drugs, its use in clinical application is limited because of its side effects in normal tissues [7–9].…”

Section: Introductionmentioning

confidence: 99%

Sirt5 Attenuates Cisplatin-Induced Acute Kidney Injury through Regulation of Nrf2/HO-1 and Bcl-2

Yang

et al. 2019

BioMed Research International

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Cisplatin- (CDDP) induced acute kidney injury (AKI) limits the clinical use of cisplatin. Several sirtuin (SIRT) family proteins are involved in AKI, while the roles of Sirt5 in cisplatin-induced AKI remain unknown. In the present study, we characterized the role and mechanism of Sirt5 in cisplatin-induced apoptosis using the human kidney 2 (HK-2) cell line. CDDP treatment decreased Sirt5 expression of HK-2 cells in a dose-dependent manner. In addition, Sirt5 overexpression enhanced the metabolic activity in CDDP-treated HK-2 cells while Sirt5 siRNA attenuated it. Forced expression of Sirt5 inhibited CDDP-induced apoptosis while Sirt5 siRNA showed the opposite effects. Accordingly, Sirt5 overexpression inhibited the level of caspase 3 cleavage and cytochrome c levels. Furthermore, we found that Sirt5 increased mitochondrial membrane potentials and ameliorated intracellular ROS production. Mitotracker Red staining indicated that Sirt5 overexpression was able to maintain the mitochondrial density during CDDP treatment. We also investigated possible downstream targets of Sirt5 and found that Sirt5 increased Nrf2, HO-1, and Bcl-2 while it decreased Bax protein expression. Sirt5 siRNA showed the opposite effect on these proteins. The levels of Nrf2, HO-1, and Bcl-2 proteins in HK-2 cells were also decreased after CDDP treatment. Moreover, Nrf2 and Bcl-2 siRNA partly abolished the protecting effect of Sirt5 on CDDP-induced apoptosis and cytochrome c release. Catalase inhibitor 3-AT also abolished the cytoprotective effect of Sirt5. Together, the results demonstrated that Sirt5 attenuated cisplatin-induced apoptosis and mitochondrial injury in human kidney HK-2 cells, possibly through the regulation of Nrf2/HO-1 and Bcl-2.

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Section: Introductionmentioning

confidence: 99%

Sirt5 Attenuates Cisplatin-Induced Acute Kidney Injury through Regulation of Nrf2/HO-1 and Bcl-2

Yang

et al. 2019

BioMed Research International

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“… 35 Tada et al have demonstrated that ENTPD6 monitors cisplatin resistance in testis and testicular cancer. 36 Rosin et al have found that DYX1C1 can indicate the poor survival in breast cancer. 37 How FCF1 and TBC1D22A act in CESC is waiting to be answered by future research.…”

Section: Discussionmentioning

confidence: 99%

Prognostic Significance of Alternative Splicing Genes in Cervical Squamous Cell Carcinoma and Endocervical Adenocarcinoma

Wang

Tang

et al. 2021

IJGM

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“…We postulate that the modulation of NTPDase expression might contribute to resistance development; however, this finding should be further investigated. The role of the NTPDases in the development of resistance has been poorly explored in the literature; however, in cisplatin-resistant testicular tumor cells (NEC-8/DDP), the expression of ENTPD6 was found to be decreased [39].…”

Section: Discussionmentioning

confidence: 99%

Imatinib mesylate affects extracellular ATP catabolism and expression of NTPDases in a chronic myeloid leukemia cell line

Willig

Vianna

Beckenkamp

et al. 2020

Purinergic Signalling

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Chronic myeloid leukemia (CML) is a myeloproliferative neoplasm, characterized by the occurrence of the t(9;22)(q34;q11) translocation. First-line therapy for CML consists of treatment with imatinib mesylate, which selectively inhibits the BCR-ABL protein by competing for its ATP-binding site. Adenine nucleotide signaling is modulated by the ectonucleotidases and this pathway is related to tumorigenic processes. Considering the relationship between ATP and cancer, we aimed to evaluate the influence of imatinib mesylate on the expressions and functions of the NTPDase and ecto-5′-nucleotidase (CD73) enzymes in imatinib-sensitive and -resistant K-562 cell lines. mRNA analysis showed that K-562 cells express all ENTPDs and NT5E. However, when treated with imatinib mesylate for 24 h, the expression of ENTPD1, -2, -3 and -5 increased, leading to a higher nucleotides hydrolysis rate. HPLC analysis identified increased ATP degradation in cells after 24 h of treatment, with consequent ADP and AMP formation, corroborating the increase in gene and protein expression of ectonucleotidases as observed in previous results. On the other hand, we observed that imatinib-resistant K-562 cells presented a decrease in nucleotide hydrolysis and expressions of ENTPD1 and -5. These results suggest an involvement of imatinib in modulating ectonucleotidases in CML that will need further investigation. Since these ectonucleotidases have important catalytic activities in the tumor microenvironment, their modulation in CML cells may represent an important therapeutic approach to regulate levels of extracellular adenine nucleotides.

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Ectonucleoside triphosphate diphosphohydrolase 6 expression in testis and testicular cancer and its implication in cisplatin resistance

Cited by 10 publications

References 19 publications

Sirt5 Attenuates Cisplatin-Induced Acute Kidney Injury through Regulation of Nrf2/HO-1 and Bcl-2

Sirt5 Attenuates Cisplatin-Induced Acute Kidney Injury through Regulation of Nrf2/HO-1 and Bcl-2

Prognostic Significance of Alternative Splicing Genes in Cervical Squamous Cell Carcinoma and Endocervical Adenocarcinoma

Imatinib mesylate affects extracellular ATP catabolism and expression of NTPDases in a chronic myeloid leukemia cell line

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