Cisplatin-induced CCL5 secretion from CAFs promotes cisplatin-resistance in ovarian cancer via regulation of the STAT3 and PI3K/Akt signaling pathways

Zhou, Bo; Sun, Chaoyang; Li, Na; Shan, Wanying; Lü, Hao; Guo, Lili; Guo, Ensong; Xia, Meng; Weng, Danhui; Li, Meng; Hu, Junbo; Ma, Ding; Chen, Gang

doi:10.3892/ijo.2016.3442

Cited by 75 publications

(66 citation statements)

References 43 publications

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“…For example, ADAM17-induced chemoresistance drug resistance in hepatocellular carcinoma cells [19]and RLIP76-induced drug resistance in pancreatic cancer cells [20]were regulated by PI3K/AKT pathway. Numerous studies have confirmed that PI3K/AKT can confer resistance to DDP-based treatment in cervical cancer[21, 22], lung cancer[22], and ovarian cancer[23]. In our study, four genes involved in this pathway, including NFKB1 , PPP2R5B , PPP2R2B , and CCNE2 , were significantly deregulated in the cisplatin-resistant cell line.…”

Section: Discussionsupporting

confidence: 74%

Transcriptome Sequencing Reveals Key Pathways and Genes Associated with Cisplatin Resistance in Lung Adenocarcinoma A549 Cells

Fang

Zhang

et al. 2017

PLoS ONE

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Acquired resistance to cisplatin-based chemotherapy frequently occurs in patients with non-small cell lung cancer, and the underlying molecular mechanisms are not well understood. The aim of this study was to investigate whether a distinct gene expression pattern is associated with acquired resistance to cisplatin in human lung adenocarcinoma. Whole-transcriptome sequencing was performed to compare the genome-wide gene expression patterns of the human lung adenocarcinoma A549 cisplatin-resistant cell line A549/DDP with those of its progenitor cell line A549. A total of 1214 differentially expressed genes (DEGs) were identified, 656 of which were upregulated and 558 were downregulated. Functional annotation of the DEGs in the Kyoto Encyclopedia of Genes and Genomes database revealed that most of the identified genes were enriched in the PI3K/AKT, mitogen-activated protein kinase, actin cytoskeleton regulation, and focal adhesion pathways in A549/DDP cells. These results support previous studies demonstrating that the pathways regulating cell proliferation and invasion confer resistance to chemotherapy. Furthermore, the results proved that cell adhesion and cytoskeleton regulation is associated with cisplatin resistance in human lung cancer. Our study provides new promising biomarkers for lung cancer prognosis and potential therapeutic targets for lung cancer treatment.

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Section: Discussionsupporting

confidence: 74%

Transcriptome Sequencing Reveals Key Pathways and Genes Associated with Cisplatin Resistance in Lung Adenocarcinoma A549 Cells

Fang

Zhang

et al. 2017

PLoS ONE

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“…Meanwhile, a recent study has illustrated that CAF-derived chemokine, namely CCL5, promotes cisplatin resistance by the regulation of PI3K/Akt signalling pathway in ovarian cancer cells [25]. Furthermore, up-regulation of GRP78 is also associated with inhibition of cell apoptosis.…”

Section: Discussionmentioning

confidence: 99%

CAF-derived HGF promotes cell proliferation and drug resistance by up-regulating the c-Met/PI3K/Akt and GRP78 signalling in ovarian cancer cells

et al. 2017

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The tumour microenvironment is a highly heterogeneous entity that plays crucial roles in cancer progression. As the most prominent stromal cell types, cancer-associated fibroblasts (CAFs) produce a variety of factors into the tumour microenvironment. In the present study, we firstly isolated CAFs from tumour tissues of the patients with ovarian cancer and demonstrated that the hepatocyte growth factor (HGF) was highly expressed in the supernatants of CAFs. CAF-derived HGF or human recombinant HGF promoted cell proliferation in human ovarian cell lines SKOV3 and HO-8910 cells. Western blotting analysis also showed that CAF-derived HGF or recombinant HGF activated c-Met/phosphoinositide 3-kinase (PI3K)/Akt and glucose-regulated protein 78 (GRP78) signalling pathways in ovarian cancer cells, and these effects could be abrogated by anti-HGF and c-Met inhibitor INCB28060. Moreover, HGF in CAF matrix attenuated paclitaxel (PAC)-caused inhibition of cell proliferation and increase in cell apoptosis through activating c-Met/PI3K/Akt and GRP78 pathways in SKOV3 and HO-8910 cells. The results in vitro were further validated in nude mice. These findings suggest that CAF-derived HGF plays crucial roles in cell proliferation and drug resistance in ovarian cancer cells.

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“…PI3K/Akt signaling pathway plays an important role in tumorigenesis and regulates critical cellular functions including survival, proliferation, and metabolism . Cisplatin‐induced CCL5 secretion derived from the CAFs may promote cisplatin resistance, which was mediated by regulation of the Stat3 and PI3K/Akt signal pathways . Moreover, endogenous Stat3 is acetylated at Lys‐685 by leukemia inhibitory factor or interleukin 6 through PI3K/Akt activation .…”

Section: Discussionmentioning

confidence: 99%

MicroRNA‐17 regulates autophagy to promote hepatic ischemia/reperfusion injury via suppression of signal transductions and activation of transcription‐3 expression

Zhang

Wang

et al. 2016

Liver Transpl

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Hepatic ischemia/reperfusion injury (IRI) represents an important clinical problem as related to liver resection or transplantation. However, the potential mechanism underlying hepatic IRI remains obscure. Recent evidence has indicated that microRNAs (miRNAs) participate in various hepatic pathophysiological processes via regulating autophagy. This relationship between MicroRNA-17 (miR-17) and hepatic autophagy prompted us to examine the role and potential mechanisms of miR-17 regulating autophagy in hepatic IRI. MiR-17 levels were significantly up-regulated after hepatic ischemia/reperfusion (IR), and the number of autophagosomes increased in response to IR. These results demonstrate that miR-17 could promote hepatic IRI as revealed by reductions in cell viability in vitro. The expression of microtubule-associated protein 1 light B II (LC3BII) was gradually up-regulated and peaked at 24 hours following reperfusion, a time point that was also associated with maximal miR-17 levels. Overexpression of miR-17 diminished signal transductions and activation of transcription-3 (Stat3) and phosphorylated Stat3 (p-Stat3) levels, an effect which promoted autophagy in response to IRI. However, low-level expressions of miR-17 were associated with increased Stat3 and p-Stat3 levels and decreased autophagy. In conclusion, high levels of miR-17 expression can function to up-regulate autophagy to aggravate hepatic IRI by suppressing Stat3 expression. Liver Transplantation 22 1697-1709 2016 AASLD.

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Cisplatin-induced CCL5 secretion from CAFs promotes cisplatin-resistance in ovarian cancer via regulation of the STAT3 and PI3K/Akt signaling pathways

Cited by 75 publications

References 43 publications

Transcriptome Sequencing Reveals Key Pathways and Genes Associated with Cisplatin Resistance in Lung Adenocarcinoma A549 Cells

Transcriptome Sequencing Reveals Key Pathways and Genes Associated with Cisplatin Resistance in Lung Adenocarcinoma A549 Cells

CAF-derived HGF promotes cell proliferation and drug resistance by up-regulating the c-Met/PI3K/Akt and GRP78 signalling in ovarian cancer cells

MicroRNA‐17 regulates autophagy to promote hepatic ischemia/reperfusion injury via suppression of signal transductions and activation of transcription‐3 expression

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