Reversal of radiation-induced cisplatin resistance in murine fibrosarcoma cells by selective modulation of the cyclic GMP-dependent transduction pathway

Eichholtz-Wirth, H

doi:10.1038/bjc.1995.326

Cited by 8 publications

(6 citation statements)

References 29 publications

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“…However, considerable evidence has suggested that cAMP and cGMP are crucial intracellular second messengers that regulate a wide variety of cellular processes including proliferation and apoptosis . Aberrant regulation of these messengers might be an important system for CDDP resistance . Moreover, among the known PDE gene families, PDE3B is the most abundantly expressed form in human leukemia cells .…”

Section: Resultsmentioning

confidence: 99%

Targeting phosphodiesterase 3B enhances cisplatin sensitivity in human cancer cells

et al. 2013

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We previously reported that human squamous cell carcinoma (SCC) cell lines refractory to cis-diaminedichloro-platinum II (cisplatin [CDDP]) had significant upregulation of the phosphodiesterase 3B gene (PDE3B), suggesting that inhibiting PDE3B suppresses CDDP resistance. shRNA-mediated PDE3B depletion in CDDP-resistant cells derived from SCC cells and Hela cells and induced CDDP sensitivity and inhibited tumor growth with elevated cyclic GMP induction resulting in upregulation of the multidrug-resistant molecule, but this did not occur in the 5-fluorouracil-resistant hepatocellular carcinoma cell lines. Furthermore, the antitumor growth effect of the combination of a PDE3B inhibitor (cilostazol) and CDDP in vivo was also greater than with either cilostazol or CDDP alone, with a significant increase in the number of apoptotic and cell growth-suppressive cancer cells in CDDP-resistance cell lines. Our results provided novel information on which to base further mechanistic studies of CDDP sensitization by inhibiting PDE3B in human cancer cells and for developing strategies to improve outcomes with concurrent chemotherapy.

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Section: Resultsmentioning

confidence: 99%

Targeting phosphodiesterase 3B enhances cisplatin sensitivity in human cancer cells

et al. 2013

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“…Resistance was associated with alterations of the cGMP-dependent transduction pathway and could be overcome either by enhanced cGMP formation (Eichholtz-Wirth, 1995a) or by heat (EichholtzWirth, 1995b). It was of interest to investigate whether a similar resistance could also be induced by radiation in human cells.…”

mentioning

confidence: 99%

Reduced expression of the ICE-related protease CPP32 is associated with radiation-induced cisplatin resistance in HeLa cells

Eichholtz-Wirth¹,

Stoetzer²,

Marx³

1997

Br J Cancer

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Summary Low-dose fractionated y-irradiation (three cycles of 5 x 2 Gy) induced cisplatin resistance in HeLa cells. The drug resistance was modest (Rf of about 2) and stable, similar to that found previously in murine cells after irradiation. In the drug-resistant HeLa-C3 cells, flow cytometric analysis revealed a decreased number of apoptotic cells compared with the parental cells. Drug resistance was associated with considerably enhanced expression of the p53 suppressor protein in HeLa-C3 cells after cisplatin exposure but seemed not to be regulated by the bcl-2-dependent pathway. Cisplatin resistance correlated with reduced expression of ICE-related proteases (interleukin-1 n-converting enzyme). Basal levels of the 45-kDa precursor ICE protein were reduced in HeLa-C3 cells, while those of the mature 60-kDa heterotetramer were similar. The CPP32 protease, a member of the ICE family with structural homology but different substrate specificity, was expressed at a lowered level. After drug exposure, there was a slight increase of CPP32 in HeLa-C3 cells, equivalent to about 45% of the level attained in the parental cells. This is in contrast to the CPP32 levels measured after irradiation, which were similar in sensitive and in resistant cells. As the radiosensitivity is unchanged in both cell lines, these results suggest that cisplatin resistance in HeLa-C3 cells is associated with alterations of a CPP32-linked apoptotic pathway, which is affected by the damage caused by cisplatin but not by irradiation. Whether these changes are dependent on the observed p53 modifications is now being studied in resistant clones.

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“…The combination of cisplatin provides a synergetic effect for radiotherapy for the reason that cisplatin could enhance the sensitivity to radiation (Boeckman et al, 2005). Interestingly, some studies have revealed that cancer cells could acquire cisplatin resistance after radiation therapy (Eichholtz-Wirth, 1995;Zhuang et al, 2019). Based on our clinical observations, the phenomenon of cisplatin resistance is commonly seen in NPC patients who also resistant to radiotherapy.…”

Section: Introductionmentioning

confidence: 70%

Radioresistant Nasopharyngeal Carcinoma Cells Exhibited Decreased Cisplatin Sensitivity by Inducing SLC1A6 Expression

Hao

Cao

et al. 2021

Front. Pharmacol.

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Cisplatin-based regimens are commonly used for the treatment of nasopharyngeal carcinoma (NPC) in patients who receive concurrent chemoradiotherapy. The sensitivity of NPC cells to cisplatin is closely associated with the efficacy of radiation therapy. In this study, we established two radioresistant NPC cell lines, HONE1-IR and CNE2-IR, and found that both cell lines showed reduced sensitivity to cisplatin. RNA-sequence analysis showed that SLC1A6 was upregulated in both HONE1-IR and CNE2-IR cell lines. Downregulation of SLC1A6 enhanced cisplatin sensitivity in these two radioresistant NPC cell lines. It was also found that the expression of SLC1A6 was induced during radiation treatment and correlated with poor prognosis of NPC patients. Notably, we observed that upregulation of SLC1A6 led to elevating level of glutamate and the expression of drug-resistant genes, resulted in reduced cisplatin sensitivity. Our findings provide a rationale for developing a novel therapeutic target for NPC patients with cisplatin resistance.

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Reversal of radiation-induced cisplatin resistance in murine fibrosarcoma cells by selective modulation of the cyclic GMP-dependent transduction pathway

Cited by 8 publications

References 29 publications

Targeting phosphodiesterase 3B enhances cisplatin sensitivity in human cancer cells

Targeting phosphodiesterase 3B enhances cisplatin sensitivity in human cancer cells

Reduced expression of the ICE-related protease CPP32 is associated with radiation-induced cisplatin resistance in HeLa cells

Radioresistant Nasopharyngeal Carcinoma Cells Exhibited Decreased Cisplatin Sensitivity by Inducing SLC1A6 Expression

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