Transcriptomic analysis reveals cell apoptotic signature modified by heparanase in melanoma cells

Song, Tian-Yi; Spillmann, Dorothe

doi:10.1111/jcmm.14349

Cited by 8 publications

(9 citation statements)

References 47 publications

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“…Finally, we showed that heparanase increased cell survival following 5-FU treatment in MCF7 human breast cancer cells via the anti-apoptotic pathway. This finding is consistent with the known anti-apoptotic effect of heparanase in melanoma cells 35 . We assume that the different molecular mechanisms of chemoresistance, which were found to be induced by heparanase, contribute synergistically to its involvement in breast cancer survival following drug therapy.…”

Section: Discussionsupporting

confidence: 92%

Heparanase: a potential marker of worse prognosis in estrogen receptor-positive breast cancer

et al. 2021

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Heparanase promotes tumor growth in breast tumors. We now evaluated heparanase protein and gene-expression status and investigated its impact on disease-free survival in order to gain better insight into the role of heparanase in ER-positive (ER+) breast cancer prognosis and to clarify its role in cell survival following chemotherapy. Using pooled analysis of gene-expression data, we found that heparanase was associated with a worse prognosis in estrogen receptor-positive (ER+) tumors (log-rank p < 10−10) and predictive to chemotherapy resistance (interaction p = 0.0001) but not hormonal therapy (Interaction p = 0.62). These results were confirmed by analysis of data from a phase III, prospective randomized trial which showed that heparanase protein expression is associated with increased risk of recurrence in ER+ breast tumors (log-rank p = 0.004). In vitro experiments showed that heparanase promoted tumor progression and increased cell viability via epithelial–mesenchymal transition, stemness, and anti-apoptosis pathways in luminal breast cancer. Taken together, our results demonstrated that heparanase is associated with worse outcomes and increased cell viability in ER+ BC.

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Section: Discussionsupporting

confidence: 92%

Heparanase: a potential marker of worse prognosis in estrogen receptor-positive breast cancer

et al. 2021

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“…It was reported that silencing HPSE expression activated apoptosis and autophagy of HCC cells [16]. Signi cantly increased apoptotic cells upon HPSE silencing was also found in melanoma cells, mediated by the activation of caspase 3 pathway [17]. We showed here a negative correlation between the activities of cleaved caspase-3 and the level of HPSE, which indicated that the caspase-3 was probably involved in HPSE regulated cell apoptosis.…”

Section: Discussionsupporting

confidence: 67%

Heparanase regulates cell proliferation, apoptosis, migration and invasion of papillary thyroid carcinoma cells with multiple signaling pathways involved

Yang¹,

Zhang²,

Chang³

et al. 2020

Preprint

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Background Heparanase (HPSE) is an endo-β-D-glucuronidase, which is found overexpressed in various human cancers. The purpose of our work was to investigate the possible role of HPSE and the involved signaling molecules in the development of papillary thyroid carcinoma (PTC). Methods The expression of HPSE was examined in 80 samples of PTC by immunohistochemistry. In cell studies, the expression plasmid of HPSE and RNA interference with shRNA specific for HPSE were used to elucidate the effects of HPSE on proliferation, apoptosis, migration and invasion in PTC cells of B-CPAP and KTC-1. The probable downstream signaling molecules of HPSE were also explored. Results 75.0% (60 out of 80) of PTC samples was detected high expression of HPSE, which was significantly correlated with tumor size, lymph node metastasis and stage status. In cell studies, the upregulation of HPSE significantly promoted cell proliferation, migration and invasion of B-CPAP and KTC-1 cells, and interfered with cell apoptosis. On the contrary, knockdown of HPSE exhibited the opposite effects. Compared with the parental cells, HPSE silencing cells showed attenuated capabilities of proliferation, migration and invasion, yet the apoptotic rate of transfected cells was increased. The activations of various signaling molecules correlated with cell biological behavior were found to be regulated by HPSE upregulation or knockdown. Conclusions Our results suggested that HPSE probably contributed to the progression and metastasis of PTC, which were associated with multiple signaling pathways. HPSE could be a potent molecular target for the therapeutic strategy of PTC.

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“…Significantly increased apoptotic cells upon HPSE silencing was also found in melanoma cells, mediated by the activation of caspase 3/PARP1 pathway [17]. We showed here a negative correlation between the activities of cleaved caspase-3/PARP and the level of HPSE, which indicated that the caspase-3/PARP was probably involved in HPSE regulated cell apoptosis.…”

Section: Discussionsupporting

confidence: 64%

Expression of heparanase regulates cell proliferation, apoptosis, migration and invasion in vitro in papillary thyroid carcinoma cells with multiple signaling pathways involved

Yang¹,

Zhang²,

Chang³

et al. 2019

Preprint

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Background Heparanase (HPSE) is an endo-β-D-glucuronidase, which is found overexpressed in various human cancers. The purpose of our work was to investigate the possible role of HPSE and the involved signaling molecules in the development of papillary thyroid carcinoma. Methods In this study, the expression plasmid of HPSE and RNA interference with shRNA specific for HPSE were used to elucidate the effects of HPSE on proliferation, apoptosis, migration and invasion in papillary thyroid carcinoma cells of B-CPAP. The probable downstream signaling molecules of HPSE were also explored. Results The results showed that upregulation of HPSE significantly promoted cell proliferation, migration and invasion of B-CPAP cells, and interfered with cell apoptosis. On the contrary, knockdown of HPSE exhibited the opposite effects. Compared with the parental cells, HPSE silencing cells showed attenuated capabilities of proliferation, migration and invasion, yet the apoptotic rate of transfected cells was increased. The activations of various signaling molecules correlated with cell biological behavior were found to be regulated by HPSE upregulation or knockdown. Conclusions Our results suggested that HPSE probably contributed to the progression and metastasis of papillary thyroid carcinoma, which were associated with multiple signaling pathways. HPSE could be a potent molecular target for the therapeutic strategy of papillary thyroid carcinoma.

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Transcriptomic analysis reveals cell apoptotic signature modified by heparanase in melanoma cells

Cited by 8 publications

References 47 publications

Heparanase: a potential marker of worse prognosis in estrogen receptor-positive breast cancer

Heparanase: a potential marker of worse prognosis in estrogen receptor-positive breast cancer

Heparanase regulates cell proliferation, apoptosis, migration and invasion of papillary thyroid carcinoma cells with multiple signaling pathways involved

Expression of heparanase regulates cell proliferation, apoptosis, migration and invasion in vitro in papillary thyroid carcinoma cells with multiple signaling pathways involved

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