IL-33 facilitates endocrine resistance of breast cancer by inducing cancer stem cell properties

Hu, Haiyan; Sun, Jiaxing; Wang, Chunhong; Bu, Xiangmao; Liu, Xiangping; Mao, Yan Ping; Wang, Haibo

doi:10.1016/j.bbrc.2017.02.080

Cited by 37 publications

(42 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The expression of IL33 in tumor tissues is depressed, but tumor stroma and serum have increased levels of IL33, suggesting the distinct functions of IL33 in cancer cells from the microenvironment [ 66 ]. IL-33 is shown to promote tumorigenesis and induce stemness in breast cancer [ 67 ]. In Apc Min/+ mice, epithelial-derived IL-33 can promote intestinal tumorigenesis [ 68 ].…”

Section: Discussionmentioning

confidence: 99%

Identification of novel gene expression signature in lung adenocarcinoma by using next-generation sequencing data and bioinformatics analysis

et al. 2017

View full text Add to dashboard Cite

Lung adenocarcinoma is one of the leading causes of cancer-related death worldwide. We showed transcriptomic profiles in three pairs of tumors and adjacent non-tumor lung tissues using next-generation sequencing (NGS) to screen protein-coding RNAs and microRNAs. Combined with meta-analysis from the Oncomine and Gene Expression Omnibus (GEO) databases, we identified a representative genetic expression signature in lung adenocarcinoma. There were 9 upregulated genes, and 8 downregulated genes in lung adenocarcinoma. The analysis of the effects from each gene expression on survival outcome indicated that 6 genes (AGR2, SPDEF, CDKN2A, CLDN3, SFN, and PHLDA2) play oncogenic roles, and 7 genes (PDK4, FMO2, CPED1, GNG11, IL33, BTNL9, and FABP4) act as tumor suppressors in lung adenocarcinoma. In addition, we also identified putative genetic interactions, in which there were 5 upregulated microRNAs with specific targets - hsa-miR-183-5p-BTNL9, hsa-miR-33b-5p-CPED1, hsa-miR-429-CPED1, hsa-miR-182-5p-FMO2, and hsa-miR-130b-5p-IL33. These 5 microRNAs have been shown to be associated with tumorigenesis in lung cancer. Our findings suggest that these genetic interactions play important roles in the progression of lung adenocarcinoma. We propose that this molecular change of genetic expression may represent a novel signature in lung adenocarcinoma, which may be developed for diagnostic and therapeutic strategies in the future.

show abstract

Section: Discussionmentioning

confidence: 99%

Identification of novel gene expression signature in lung adenocarcinoma by using next-generation sequencing data and bioinformatics analysis

et al. 2017

View full text Add to dashboard Cite

show abstract

“…In consistent with these findings, IL-33 signaling promoted membrane GLUT1 localization and glycolysis of NSCLC cells [ 25 ]. IL-33 facilitated endocrine resistance of breast cancer by inducing cancer stem cell properties [ 52 ]. Of important, blockade of IL-33 restricted tumor progression of human NSCLC xenograft in immune-deficient mice [ 53 ].…”

Section: Discussionmentioning

confidence: 99%

“…NSCLC cells were seeded at 1×10 5 cells/ml at ultralow attachment plates and cultured for 7 days. MS with a diameter ≥ 50μm were counted and MS-forming efficiency (MFE) was calculated by dividing the number of MS with original number of seeded cells [ 52 ].…”

Section: Methodsmentioning

confidence: 99%

Gram-negative bacteria facilitate tumor progression through TLR4/IL-33 pathway in patients with non-small-cell lung cancer

et al. 2018

View full text Add to dashboard Cite

Non-small-cell lung cancer (NSCLC) accounts for the most cases in clinical lung cancer patients. Patients with NSCLC are often diagnosed in advanced stage and frequently infected with gram-negative bacteria. Pulmonary infection with gram-negative bacteria is the most frequent postoperative complication in NSCLC patients. While accumulating evidence indicate an involvement of gram-negative bacteria in NSCLC progression, the underlying mechanisms remain largely unknown. Herein, we explored the effect of gram-negative bacteria on tumor progression using tumor cells from NSCLC patients. We observed that infection with gram-negative bacteria predicted advanced stages and decreased time interval to recurrence of NSCLC patients. Incubation of NSCLC cells with gram-negative bacteria promoted their growth and metastasis. Mechanistically, gram-negative bacteria activated Toll-like receptor 4 (TLR4) signaling in NSCLC cells, leading to increased mRNA and protein expression of interleukin 33 (IL-33) through MyD88-dependent pathway. Knockdown of IL-33 abrogated the contribution of gram-negative bacteria to NSCLC progression by regulating cancer metabolic activities and stem cell properties. In NSCLC patients, higher TLR4 expression was associated with increased IL-33 expression, Ki-67 proliferation index and CD133 expression in those with gram-negative bacterial infection. These findings shed new light on the molecular mechanisms underlie gram-negative bacteria mediated tumor progression and provide clues for innovative therapeutic explorations for NSCLC patients.

show abstract

“…An additional mechanism states that IL-33 contributes to tumor immune evasion by promoting the expansion and immunosuppressive function of myeloid suppressor cells. These findings consider IL-33 as a pro-cancer cytokine important in the development of breast cancer [18]. The expression of IL-33 in tumor cells predicts a higher activity of ALDH, a greater expression of SOX2, a decrease in the expression of the estrogen receptor and therefore favors resistance to tamoxifen [18].…”

Section: Interleukin 33 (Il-33)mentioning

confidence: 94%

“…IL-33 is constitutively expressed in epithelial barrier tissues and lymphoid organs, maintaining the barrier function under normal conditions, and is released as a warning signal of cell damage or stress. In patients with breast cancer, serum IL-33 is significantly higher and correlates with levels of VEGF, MMP-11 and PDGF-C that indicate a poor prognosis [18]. The expression of IL-33 in tumor tissues participates in the prediction of aggressive phenotype of cancer cells and increased involvement of lymph node involvement in patients with breast cancer, Likewise, signaling of the IL-33 / ST2 complex promotes the progression of breast cancer through the support of inflammation and tumorigenesis, facilitating the expression of proangiogenic VEGF and attenuating tumor necrosis [18].…”

Section: Interleukin 33 (Il-33)mentioning

confidence: 99%

Genes and proteins associated with chemotherapeutic resistance in breast cancer

Linares¹,

Benítez²,

Avila³

2018

Calcified Constrictive Pericarditis Treated With Ultrasonic Devices

View full text Add to dashboard Cite

Breast cancer is the main type of cancer that affects women in the world. Treatment with chemotherapeutic agents for this type of cancer depends to a large extent on the phenotypic characteristics that appear in the tumor, such as some receptors. The treatment of breast cancer is complex since not all patients respond adequately to it and this is partly due to mechanisms of resistance to treatment. The resistance either acquired or intrinsic to chemotherapeutics against breast cancer is related to multiple genes and proteins that are actively involved in the development of resistance mechanisms, which may be inhibiting the binding of the drug to the target receptor, inhibiting the gene expression of the receptors, activating signaling pathways, inducing the action of transporters that expel the drug from the cell, etc. As a result of this review, the mechanisms of chemotherapeutic resistance in breast cancer derived from genes and proteins related to say disease are described, including genes related to different types of breast cancer, as well as with different therapeutic strategies. These genes and their products of expression include a wide range of interactions and activations of signalling pathways that trigger a poor response to treatment, which translates into a worse prognosis, higher risk of prevalence and death, favouring breast cancer to be the main cause of cancer death in women. Objective: Conduct an updated review of genes and proteins, that have been associated with conferring resistance to the different chemotherapeutic agents used for the treatment of breast cancer, including the mechanism of resistance and the type of cancer in which it is generated. Method: The search for indexed articles in the PubMed (https://www.ncbi.nlm.nih.gov/pubmed/) and ScienceDirect (http://www.sciencedirect.com) databases was performed, using the words "Breast cancer resistance" as a search criterion, articles published in the period 2015-2017 were selected.

show abstract

IL-33 facilitates endocrine resistance of breast cancer by inducing cancer stem cell properties

Cited by 37 publications

References 32 publications

Identification of novel gene expression signature in lung adenocarcinoma by using next-generation sequencing data and bioinformatics analysis

Identification of novel gene expression signature in lung adenocarcinoma by using next-generation sequencing data and bioinformatics analysis

Gram-negative bacteria facilitate tumor progression through TLR4/IL-33 pathway in patients with non-small-cell lung cancer

Genes and proteins associated with chemotherapeutic resistance in breast cancer

Contact Info

Product

Resources

About