Retraction Note: IL-6 secreted by cancer-associated fibroblasts induces tamoxifen resistance in luminal breast cancer

Sun, Xin; Mao, Yihua; Zu, Lidong; Hao, Ming‐Hong; Cheng, Guangcun; Qu, Qing; Dong, Chao; Keller, Eleanor; X, Chen; Shen, Kui; Wang, J

doi:10.1038/onc.2014.224

Cited by 36 publications

(20 citation statements)

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“…In our study the result confirm that ERβ play a vital role in lung cancer. Meanwhile, IL6 is associated with cancer development, including lung cancer [ 15 , 16 , 42 ]. Ectopic expression of IL-6 is correlated with tumor progression and overall survival in patients with NSCLC [ 15 , 18 ].…”

Section: Discussionmentioning

confidence: 99%

17β-estradiol upregulates IL6 expression through the ERβ pathway to promote lung adenocarcinoma progression

Huang

Zhang

Liao

et al. 2018

J Exp Clin Cancer Res

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BackgroundIn non-small cell lung cancer (NSCLC), estrogen (E2) significantly promotes NSCLC cell growth via estrogen receptor beta (ERβ). Discovery and elucidation of the mechanism underlying estrogen-promoted NSCLC progression is critical for effective preventive interventions. IL6 has been demonstrated to be involved in the development, progression and metastasis in several cancers and IL6 overexpression is associated with poor prognosis in NSCLC. However, the exact role played by IL6 in estrogen-promoted NSCLC progress remain unknown. Here, we evaluated the expression and biological effects of IL6 in NSCLC cells when treated with E2 and explored the underlying mechanism of IL6 in E2-promoted NSCLC progression.MethodsExpression of ERβ/IL6 in 289 lung cancer samples was assessed by immunohistochemistry. Matched samples of metastatic lymph node and primary tumor tissues were used to quantify the expression of ERβ/IL6 by western blot. Expression levels of IL6 in NSCLC cells were quantified by western blotting, ELISA, and immunofluorescence staining. The effects of IL6 stimulated by E2 on cell malignancy were evaluated using CCK8, colony formation, wound healing and transwell. Furthermore, overexpression and knockdown ERβ constructs were constructed to measure the expression of IL6. The effects of IL6 stimulated by E2 on tumor growth were evaluated using a urethane-induced adenocarcinoma model. In addition, a xenograft mouse model was used to observe differences in ERβ subtype tumor growth with respect to IL6 expression.ResultsIL6/ERβ expression were significantly increased in lung cancer. Higher IL6/ERβ expression was associated with decreased differentiation or increased metastasis. IL6 was an independent prognostic factor for overall survival (OS), higher IL6 expression was associated with decreased OS. Furthermore, ERβ regulates IL6 expression via MAPK/ERK and PI3K/AKT pathways when stimulated by E2 and promotes cell malignancy in vitro and induced tumor growth in vivo. Finally we confirm that ERβ isolation 1/5 is essential for E2 promotion of IL6 expression, while ERβ2 not.ConclusionsOur findings demonstrate that E2 stimulates IL6 expression to promote lung adenocarcinoma progression through the ERβ pathway. We also clarify the difference in each ERβ subtype for E2 promoting IL6 expression, suggesting that ERβ/IL6 might be potential targets for prognostic assessment and therapeutic intervention in lung cancer.Electronic supplementary materialThe online version of this article (10.1186/s13046-018-0804-5) contains supplementary material, which is available to authorized users.

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Section: Discussionmentioning

confidence: 99%

17β-estradiol upregulates IL6 expression through the ERβ pathway to promote lung adenocarcinoma progression

Huang

Zhang

Liao

et al. 2018

J Exp Clin Cancer Res

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“…Chemotherapy-treated CAFs maintain cancer-initiating cells (CICs) and their drug resistance through secretion of IL-17A [ 108 ]. In breast cancer, IL-6 secretion by CAFs promotes tamoxifen resistance through degradation of ER-α [ 109 ].…”

Section: The Role Of Cafsmentioning

confidence: 99%

Cancer-Associated Fibroblasts: Their Characteristics and Their Roles in Tumor Growth

Shiga

Hara

Nagasaki

et al. 2015

Cancers

667

538

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Cancer tissues are composed of cancer cells and the surrounding stromal cells (e.g., fibroblasts, vascular endothelial cells, and immune cells), in addition to the extracellular matrix. Most studies investigating carcinogenesis and the progression, invasion, metastasis, and angiogenesis of cancer have focused on alterations in cancer cells, including genetic and epigenetic changes. Recently, interactions between cancer cells and the stroma have attracted considerable attention, and increasing evidence has accumulated on this. Several researchers have gradually clarified the origins, features, and roles of cancer-associated fibroblasts (CAFs), a major component of the cancer stroma. CAFs function in a similar manner to myofibroblasts during wound healing. We previously reported the relationship between CAFs and angiogenesis. Interleukin-6 (IL-6), a multifunctional cytokine, plays a central role in regulating inflammatory and immune responses, and important roles in the progression, including proliferation, migration, and angiogenesis, of several cancers. We showed that CAFs are an important IL-6 source and that anti-IL-6 receptor antibody suppressed angiogenesis and inhibited tumor-stroma interactions. Furthermore, CAFs contribute to drug-resistance acquisition in cancer cells. The interaction between cancer cells and the stroma could be a potential target for anti-cancer therapy.

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“…In breast cancer, IL-6 from CAFs interacts with breast tumor cells to induce EMT and create a cancer stem cell subpopulation. This leads to resistance to tamoxifen, highly suggestive of a role for CAF-derived IL-6 in recurrence following conventional therapy [ 114 ].…”

Section: Section 2 : Opn Modifies the Microenvimentioning

confidence: 99%

Osteopontin—A Master Regulator of Epithelial-Mesenchymal Transition

Kothari

Arffa

Chang

et al. 2016

JCM

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Osteopontin (OPN) plays an important functional role in both physiologic and pathologic states. OPN is implicated in the progression of fibrosis, cancer, and metastatic disease in several organ systems. The epithelial-mesenchymal transition (EMT), first described in embryology, is increasingly being recognized as a significant contributor to fibrotic phenotypes and tumor progression. Several well-established transcription factors regulate EMT and are conserved across tissue types and organ systems, including TWIST, zinc finger E-box-binding homeobox (ZEB), and SNAIL-family members. Recent literature points to an important relationship between OPN and EMT, implicating OPN as a key regulatory component of EMT programs. In this review, OPN’s interplay with traditional EMT activators, both directly and indirectly, will be discussed. Also, OPN’s ability to restructure the tissue and tumor microenvironment to indirectly modify EMT will be reviewed. Together, these diverse pathways demonstrate that OPN is able to modulate EMT and provide new targets for directing therapeutics.

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Retraction Note: IL-6 secreted by cancer-associated fibroblasts induces tamoxifen resistance in luminal breast cancer

Cited by 36 publications

References 0 publications

17β-estradiol upregulates IL6 expression through the ERβ pathway to promote lung adenocarcinoma progression

17β-estradiol upregulates IL6 expression through the ERβ pathway to promote lung adenocarcinoma progression

Cancer-Associated Fibroblasts: Their Characteristics and Their Roles in Tumor Growth

Osteopontin—A Master Regulator of Epithelial-Mesenchymal Transition

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