Blockage of cisplatin-induced autophagy sensitizes cervical cancer cells to cisplatin

Wm, Lin; Zg, Li

doi:10.4238/2015.december.14.18

Cited by 20 publications

(15 citation statements)

References 22 publications

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“…Cisplatin induced autophagy in a concentration-dependent manner in the examined cells, as demonstrated by the western blot results for the autophagy markers LC3-I, LC3-II and p62. This compound has previously been demonstrated to induce autophagy in various types of cancer cells, such as ovarian cancer cells and osteosarcoma cancer cells (35,36), and another study indicated that autophagy serves a protective role in cisplatin resistance (34). The results of the present study demonstrated that the blockade of autophagy promoted cisplatin-induced cell death in SKOV3 and SKOV3/DDP cells, and partially re-sensitized cisplatin-resistant SKOV3/DDP cells.…”

Section: Discussionsupporting

confidence: 68%

Downregulation of BAG3 attenuates cisplatin resistance by inhibiting autophagy in human epithelial ovarian cancer cells

et al. 2019

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Epithelial ovarian cancer (EOC) is one of the most common malignant gynecological tumors. Interval cytoreductive surgery and cisplatin-based chemotherapy are the standard treatments. However, acquired resistance to cisplatin presents a major challenge for improving the overall survival and prognosis of patients. Recent evidence indicates that cytoprotective functions of autophagy in cancer cells is a potential mechanism for chemoresistance. The present study aimed to investigate the mechanisms responsible for cisplatin resistance in EOC cell lines. The results revealed that cisplatin activated autophagy, measured by an increase in the expression of LC3-II by western blot analysis, protecting ovarian cancer cells from cisplatin toxicity. The present study also identified Bcl-2-associated athanogene 3 (BAG3) as a novel autophagy regulator that serves a role in cisplatin resistance. Treatment with cisplatin was observed to enhance BAG3 expression in parental and cisplatin-resistant ovarian cancer cell lines, and the downregulation of BAG3 blocked cisplatin-induced autophagy, thereby increasing cisplatin sensitivity in the EOC cell lines. In conclusion, BAG3 attenuates cisplatin resistance by inhibiting autophagy, suggesting that downregulation of BAG3 may be a useful therapeutic strategy to overcome cisplatin resistance by preventing cytoprotective autophagy in EOC.

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Section: Discussionsupporting

confidence: 68%

Downregulation of BAG3 attenuates cisplatin resistance by inhibiting autophagy in human epithelial ovarian cancer cells

et al. 2019

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“…91,92 A recent study suggested that Cis induces autophagy in HeLa cells via upregulating the formation of autophagic vesicles, promoting the conversion of LCI to LCII and increasing the expression of the autophagy-related ATG7 gene. 82 Our findings provide evidence that the autophagy induced by Cis …”

Section: Combination Of Cis and Rgo-agnps Induces Accumulation Of Autmentioning

confidence: 51%

Combination of graphene oxide–silver nanoparticle nanocomposites and cisplatin enhances apoptosis and autophagy in human cervical cancer cells

Yuan¹,

Gurunathan²

2017

IJN

111

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Background Cisplatin (Cis) is a widely used chemotherapeutic drug for treating a variety of cancers, due to its ability to induce cell death in cancer cells significantly. Recently, graphene and its modified nanocomposites have gained much interest in cancer therapy, due to their unique physicochemical properties. The objective of this study was to investigate the combination effect of Cis and a reduced graphene oxide–silver nanoparticle nanocomposite (rGO-AgNPs) in human cervical cancer (HeLa) cells. Materials and methods We synthesized AgNPs, rGO, and rGO-AgNP nanocomposites using C-phycocyanin. The synthesized nanomaterials were characterized using various analytical techniques. The anticancer properties of the Cis, rGO-AgNPs, and combination of Cis and rGO-AgNPs were evaluated using a series of cellular assays, such as cell viability, cell proliferation, LDH leakage, reactive oxygen species generation, and cellular levels of oxidative and antioxidative stress markers such as malondialdehyde, glutathione, SOD, and CAT. The expression of proapoptotic, antiapoptotic, and autophagy genes were measured using real-time reverse-transcription polymerase chain reaction. Results The synthesized AgNPs were well dispersed, homogeneous, and spherical, with an average size of 10 nm and uniformly distributed on graphene sheets. Cis, GO, rGO, AgNPs, and rGO-AgNPs inhibited cell viability in a dose-dependent manner. The combination of Cis and rGO-AgNPs showed significant effects on cell proliferation, cytotoxicity, and apoptosis. The combination of Cis and rGO-AgNPs had more pronounced effects on the expression of apoptotic and autophagy genes, and also significantly induced the accumulation of autophagosomes and autophagolysosomes, which was associated with the generation of reactive oxygen species. Conclusion Our findings substantiated rGO-AgNPs strongly potentiating Cis-induced cytotoxicity, apoptosis, and autophagy in HeLa cells, and hence rGO-AgNPs could be potentially applied to cervical cancer treatment as a powerful synergistic agent with Cis or any other chemotherapeutic agents.

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“…Autophagy is a process in which cellular material transferred into lysosomes for degradation and amount of studies illustrated that autophagy plays extremely important roles in cancer cells [32]. In addition, LC3-I and LC3-II are two important marker factors in autophagy and autophagy promoted the conversion of LC3-I to LC3-II [33]. Transfection with EGFP-LC-3, the phagosome-specific marker, could trace the change of LC-3, by which to determine the situation of autophagy [34].…”

Section: Discussionmentioning

confidence: 99%

ASF1A regulates H4 ^Y72 phosphorylation and promotes autophagy in colon cancer cells via a kinase activity

Qiu

Wang

Chu

et al. 2019

Artificial Cells, Nanomedicine, and Biotechnology

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Colon cancer is one of the most malignant cancers. Histone modification is closely related to tumour development. Our study explored the functions of anti-silencing function 1A (ASF1A) on H4 Y72ph in colon cancer cells. Colon cancer cell lines and clinical specimens were obtained and/or transfected with full length ASF1A or interference mRNA to mimic or silence of ASF1A expression. Immunoprecipitation and GST pull down was used to target targeting ASF1A or H4 Y72ph. Cells were transfected with H4 WTor H4 Y72F-expressing. An in vitro kinase activity assay was set to determine whether ASF1A could phosphorylate H4. The severity of autophagy was measured by detecting number of autophagosomes, number of EGFP-LC3, LC3-II/I, percentage of degradation and expression of autophagy associated gene (ATG). ASF1A positively regulated H4 Y72ph ; Immunoprecipitation assay and GST pull down results showed that ASF1A interacted directly with H4. In addition, ASF1A silence inhibited autophagosomes number, EGFP-LC3 number, LC3-II/I, percentage of degradation and ATG expression. Moreover, H4 Y72F impaired the promoting autophagy effects of ASF1A. The ASF1A-H4 Y72ph axis promoted colon cancer autophagy via transcriptional regulation of ATG genes. ASF1A regulated H4 Y72ph and promotes autophagy in colon cancer cells via a kinase activity through regulation of ATG.

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Blockage of cisplatin-induced autophagy sensitizes cervical cancer cells to cisplatin

Cited by 20 publications

References 22 publications

Downregulation of BAG3 attenuates cisplatin resistance by inhibiting autophagy in human epithelial ovarian cancer cells

Downregulation of BAG3 attenuates cisplatin resistance by inhibiting autophagy in human epithelial ovarian cancer cells

Combination of graphene oxide–silver nanoparticle nanocomposites and cisplatin enhances apoptosis and autophagy in human cervical cancer cells

ASF1A regulates H4 ^Y72 phosphorylation and promotes autophagy in colon cancer cells via a kinase activity

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Blockage of cisplatin-induced autophagy sensitizes cervical cancer cells to cisplatin

Cited by 20 publications

References 22 publications

Downregulation of BAG3 attenuates cisplatin resistance by inhibiting autophagy in human epithelial ovarian cancer cells

Downregulation of BAG3 attenuates cisplatin resistance by inhibiting autophagy in human epithelial ovarian cancer cells

Combination of graphene oxide&ndash;silver nanoparticle nanocomposites and cisplatin enhances apoptosis and autophagy in human cervical cancer cells

ASF1A regulates H4 Y72 phosphorylation and promotes autophagy in colon cancer cells via a kinase activity

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Combination of graphene oxide–silver nanoparticle nanocomposites and cisplatin enhances apoptosis and autophagy in human cervical cancer cells

ASF1A regulates H4 ^Y72 phosphorylation and promotes autophagy in colon cancer cells via a kinase activity