Luteinizing hormone inhibits cisplatin-induced apoptosis in human epithelial ovarian cancer cells

Xia, Lingfang; Wen, Hao; Han, Xiaotian; Tang, Jia; Huang, Yan

doi:10.3892/ol.2016.4122

Cited by 5 publications

(6 citation statements)

References 21 publications

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“…Most mice exhibited some of these symptoms, however, mice in the control and LH groups exhibited the most severe symptoms. Seeing as mice in these two groups did not receive cisplatin chemotherapy, this was in line with expectations (18). When most mice in the control and LH groups presented with symptoms and became moribund, all the mice in the experiment were sacrificed immediately.…”

Section: Luteinizing Hormone Compromises the In Vivo Anti-tumor Effecsupporting

confidence: 74%

“…FSH has been identified to serve a function in the development and progression of ovarian cancer in vitro and in vivo (21,25). However, previous studies have identified that LH is able to inhibit apoptosis and facilitate angiogenesis in vitro (26)(27)(28), and therefore the effect of LH in vivo is worth investigating. In the present study, two epithelial ovarian cancer cell lines, HeyA8 and SKOV3ip1, were implanted into nude mice and the effect of exogenous LH was detected on the cisplatin anti-tumor activity.…”

Section: Discussionmentioning

confidence: 99%

“…LH may inhibit cisplatin-induced apoptosis in vitro (18). Therefore, the present study used epithelial ovarian cancer cells to determine whether LH impairs the in vivo anti-tumor effect of cisplatin in xenograft nude mice, at least in part, by inhibiting the pro-apoptotic activity of cisplatin.…”

Section: Introductionmentioning

confidence: 99%

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Luteinizing hormone compromises the inï¿½vivo anti-tumor effect of cisplatin on human epithelial ovarian cancer cells

et al. 2017

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Abstract. Platinum-based chemotherapy is the most common therapeutic regimen used to treat patients with ovarian cancer. However, the emergence of drug resistance to platinum compromises the clinical success of this treatment. Epithelial ovarian cancer is usually accompanied by an increased level of luteinizing hormone (LH). Therefore, the effect of LH on platinum resistance requires further investigation. In the current study, the effect of cisplatin and/or LH on platinum resistance was examined using the SKOV3ip1 and HeyA8 models. Following therapy, tumors were examined for proliferation (ki67) and apoptosis (cleaved caspase-3). Cisplatin alone and in combination with LH significantly inhibited tumor growth in SKOV3ip1-and HeyA8-implanted mice. Treatment with LH alone had minimal effect in the models. However, treatment with cisplatin combined with LH was less effective than treatment with cisplatin alone. Additionally, ki67 counts were significantly increased and cleaved caspase-3 counts were significantly reduced in mice treated with cisplatin combined with LH compared with mice treated with cisplatin alone. Such results indicate that LH weakens the anti-tumor effect of cisplatin in vivo and that LH may contribute to the development of drug resistance to cisplatin in ovarian cancer.

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Section: Luteinizing Hormone Compromises the In Vivo Anti-tumor Effecsupporting

confidence: 74%

Section: Discussionmentioning

confidence: 99%

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Luteinizing hormone compromises the inï¿½vivo anti-tumor effect of cisplatin on human epithelial ovarian cancer cells

et al. 2017

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“…PDCD1, often known as PD-1, is the member that has been most extensively studied and shown to negatively regulate T cell responses, in collaboration with its two ligands, PD-L1 and PD-L2 (51)(52)(53). In addition to PDCD5, other programmed cell death proteins are also known to play important roles in apoptosis and/or cell cycle progression (54)(55)(56)(57), and are also dysregulated in many types of human cancers (13,16,(58)(59)(60)(61)(62)(63). Opposite to what we observed for PDCD5, depletion of PDCD2 in human acute leukemia cells impairs their proliferation, induces cell cycle arrest and p53 activation while overexpression of PDCD2 facilitates cell growth in cancers (55,64).…”

Section: Discussionmentioning

confidence: 99%

PDCD5 regulates cell proliferation, cell cycle progression and apoptosi

Hong-xin

Wang

et al. 2017

Oncol Lett

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Abstract. Programmed cell death (PDCD)5 is cloned from human leukemia cell line TF-1. PDCD5 is one of the members of the programmed cell death protein family that is frequently involved in tumor growth and apoptosis. To investigate the molecular and cellular functions of PDCD5, the present study established a PDCD5 stably overexpressing A431 cell line and examined the role of PDCD5 in cell proliferation, cell cycle progression and apoptosis. The data demonstrated that overexpression of PDCD5 significantly inhibited cell proliferation, induced cell cycle arrest at G2/M phase and apoptosis in A431 cells. The expression profiles of certain key regulators of these cellular events were further investigated, including P53, B cell lymphoma (BCL)-2, BCL-2 associated X protein (BAX) and caspase (CASP)3. The data demonstrated that at the transcript and protein levels, P53, BAX and CASP3 were all upregulated in the PDCD5 stably overexpressing A431 cells whereas BCL-2 was downregulated, indicating that PDCD5 acts as an important upstream regulator of P53, BCL-2, BAX and CASP3. The data suggest that PDCD5 regulates cell proliferation, cell cycle progression and apoptosis in A431 cells. PDCD5 may be a novel tumor suppressor gene, and may be potentially used for cancer treatment in the future.

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“…The amplification of LH action on granulosa cells may affect folliculogenesis. High LH may cause inhibition of apoptosis in granulosa cells in PCOS, as LH was reported to prevent cisplatininduced apoptosis in ovarian cancer or apoptosis in oocytes (22,23). Under this condition, apoptotic and or proliferation regulator show aberrant expression.…”

Section: Discussionmentioning

confidence: 99%

Whole Genome Transcriptomic Analysis of Ovary Granulosa Cells Revealed an Anti-Apoptosis Regulatory Gene DLGAP5 in Polycystic Ovary Syndrome

Deng

Song

et al. 2022

Front. Endocrinol.

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The mechanisms underlining pathogenesis of polycystic ovary syndrome (PCOS) remain largely unknown. Dysfunction of ovarian granulosa cells plays an important role. The present study performed the lncRNA and mRNA profiling by whole genome transcriptomic sequencing of ovary granulosa cells from women with PCOS and investigated the potential role of differentially expressed gens (DEGs) in the pathomechanism of PCOS. In total, 1,936 DEGs (30 upregulated and 1,906 downregulated mRNAs and lncRNAs) were identified in the ovary granulosa cells between control and PCOS group. Functional enrichment analysis showed that DEGs were mainly associated with cytokine–cytokine receptor interaction, neuroactive ligand–receptor interaction, and olfactory transduction. qRT-PCR validated the upregulation of DLGAP5 mRNA in ovary from PCOS group when compared to control group. Immunostaining and TUNEL assays showed that DLGAP5 protein level was increased while apoptosis was decreased in follicles of ovary in PCOS group. In vitro functional assays showed that DLGPA5 knockdown repressed viability and proliferation, but enhanced apoptosis and disrupted cell cycle in granulosa cells; while DLGAP5 overexpression had the opposite effects in granulosa cells. In conclusion, the study showed differentially expressed lncRNA and mRNA profile in the granulosa cells in ovaries of PCOS. Functional results demonstrated that DLGAP5 is a dysregulated candidate gene in the pathogenesis of PCOS, especially granulosa cell apoptosis and proliferation.

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Luteinizing hormone inhibits cisplatin-induced apoptosis in human epithelial ovarian cancer cells

Cited by 5 publications

References 21 publications

Luteinizing hormone compromises the inï¿½vivo anti-tumor effect of cisplatin on human epithelial ovarian cancer cells

Luteinizing hormone compromises the inï¿½vivo anti-tumor effect of cisplatin on human epithelial ovarian cancer cells

PDCD5 regulates cell proliferation, cell cycle progression and apoptosi

Whole Genome Transcriptomic Analysis of Ovary Granulosa Cells Revealed an Anti-Apoptosis Regulatory Gene DLGAP5 in Polycystic Ovary Syndrome

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