Cancer-Associated Fibroblasts Promote the Chemo-resistance in Gastric Cancer through Secreting IL-11 Targeting JAK/STAT3/Bcl2 Pathway

Ma, Jun; Song, Xiao; Xu, Xiaorong; Mou, Yiping

doi:10.4143/crt.2018.031

Cited by 59 publications

(48 citation statements)

References 34 publications

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“…Similar results were observed for oxaliplatin [168]. In vitro studies revealed that IL-11 increased chemoresistance through gp130/JAK/STAT3/BCL-2-mediated anti-apoptosis signaling pathway [169].…”

Section: Mechanisms Of Chemoresistance Type 6 (Moc-6)supporting

confidence: 80%

Molecular Bases of Mechanisms Accounting for Drug Resistance in Gastric Adenocarcinoma

Marin

Perez‐Silva

Macı́as

et al. 2020

Cancers

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Gastric adenocarcinoma (GAC) is the most common histological type of gastric cancer, the fifth according to the frequency and the third among the deadliest cancers. GAC high mortality is due to a combination of factors, such as silent evolution, late clinical presentation, underlying genetic heterogeneity, and effective mechanisms of chemoresistance (MOCs) that make the available antitumor drugs scarcely useful. MOCs include reduced drug uptake (MOC-1a), enhanced drug efflux (MOC-1b), low proportion of active agents in tumor cells due to impaired pro-drug activation or active drug inactivation (MOC-2), changes in molecular targets sensitive to anticancer drugs (MOC-3), enhanced ability of cancer cells to repair drug-induced DNA damage (MOC-4), decreased function of pro-apoptotic factors versus up-regulation of anti-apoptotic genes (MOC-5), changes in tumor cell microenvironment altering the response to anticancer agents (MOC-6), and phenotypic transformations, including epithelial-mesenchymal transition (EMT) and the appearance of stemness characteristics (MOC-7). This review summarizes updated information regarding the molecular bases accounting for these mechanisms and their impact on the lack of clinical response to the pharmacological treatment currently used in GAC. This knowledge is required to identify novel biomarkers to predict treatment failure and druggable targets, and to develop sensitizing strategies to overcome drug refractoriness in GAC.

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Section: Mechanisms Of Chemoresistance Type 6 (Moc-6)supporting

confidence: 80%

Molecular Bases of Mechanisms Accounting for Drug Resistance in Gastric Adenocarcinoma

Marin

Perez‐Silva

Macı́as

et al. 2020

Cancers

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“…Knockdown of IL-11 in pancreatic cancer cell lines resulted in reduced expression of MMP2 and MMP9 and a 50% reduction in invasive capacity [200]. These results suggest that IL-11 may have a pro-tumorigenic effect in pancreatic cancer, similar to its roles in colorectal [201], gastric [202], and breast [203] cancers.…”

Section: Il-11 May Have a Pro-tumorigenic Role In Pdacmentioning

confidence: 75%

Emerging roles for the IL-6 family of cytokines in pancreatic cancer

2020

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Pancreatic cancer has one of the poorest prognoses of all malignancies, with little improvement in clinical outcome over the past 40 years. Pancreatic ductal adenocarcinoma is responsible for the vast majority of pancreatic cancer cases, and is characterised by the presence of a dense stroma that impacts therapeutic efficacy and drives pro-tumorigenic programs. More specifically, the inflammatory nature of the tumour microenvironment is thought to underlie the loss of anti-tumour immunity and development of resistance to current treatments. Inflammatory pathways are largely mediated by the expression of, and signalling through, cytokines, chemokines, and other cellular messengers. In recent years, there has been much attention focused on dual targeting of cancer cells and the tumour microenvironment. Here we review our current understanding of the role of IL-6, and the broader IL-6 cytokine family, in pancreatic cancer, including their contribution to pancreatic inflammation and various roles in pancreatic cancer pathogenesis. We also summarise potential opportunities for therapeutic targeting of these pathways as an avenue towards combating poor patient outcomes.

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“…Studies have demonstrated that the JAK/STAT3 signaling pathway contributes to cell survival and chemotherapeutic resistance in cancers [ 23 , 24 ]. Furthermore, it enhances the development of CSC-like characteristics [ 25 ].…”

Section: Discussionmentioning

confidence: 99%

Glycochenodeoxycholic acid induces stemness and chemoresistance via the STAT3 signaling pathway in hepatocellular carcinoma cells

Shi

Yang

et al. 2020

Aging

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The poor prognosis of hepatocellular carcinoma (HCC) is primarily attributed to its high frequency of recurrence and resistance to chemotherapy. Epithelial-to-mesenchymal transition (EMT) and the acquisition of cancer stem cells (CSCs) are the fundamental drivers of chemoresistance in HCC. Glycochenodeoxycholic acid (GCDC), a component of bile acid (BA), has been reported to induce necrosis in primary human hepatocytes. In the present work, we investigated the function of GCDC in HCC chemoresistance. We found that GCDC promoted chemoresistance in HCC cells by down-regulating and up-regulating the expression of apoptotic and anti-apoptotic genes, respectively. Furthermore, GCDC induced the EMT phenotype and stemness in HCC cells and activated the STAT3 signaling pathway. These findings reveal that GCDC promotes chemoresistance in HCC by inducing stemness via the STAT3 pathway and could be a potential target in HCC chemotherapy.

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Cancer-Associated Fibroblasts Promote the Chemo-resistance in Gastric Cancer through Secreting IL-11 Targeting JAK/STAT3/Bcl2 Pathway

Abstract: Our results demonstrated that IL-11 contributed to the obtain of resistance to chemotherapy drugs through gp130/JAK/STAT3/Bcl2 pathway, and targeting the IL-11 signaling pathway induced by fibroblasts might be a promising strategy to overcome the multi-drugs resistant cancer in clinic.

Cited by 59 publications

References 34 publications

Molecular Bases of Mechanisms Accounting for Drug Resistance in Gastric Adenocarcinoma

Molecular Bases of Mechanisms Accounting for Drug Resistance in Gastric Adenocarcinoma

Emerging roles for the IL-6 family of cytokines in pancreatic cancer

Glycochenodeoxycholic acid induces stemness and chemoresistance via the STAT3 signaling pathway in hepatocellular carcinoma cells

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