TBX21 predicts prognosis of patients and drives cancer stem cell maintenance via the TBX21–IL-4 pathway in lung adenocarcinoma

Zhao, Shuangtao; Shen, Wenzhi; Yu, Jiangyong; Wang, Lühua

doi:10.1186/s13287-018-0820-6

Cited by 21 publications

(32 citation statements)

References 40 publications

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“…Shirota et al determined that IL-4 from T follicular helper cells downregulated antitumor immunity by inducing myeloid cells to differentiate into M2 macrophages [126], corroborating the cooperation of IL-4 and TAMs in modulating tumor progression in the TME. In addition to the signaling transduction mentioned above multiple tumor-promoting functions mediated by IL-4 are supposed to be triggered by the activation of transcription factors like T-box 21 in lung carcinogenesis [127]. IL-4-induced gene 1 selectively expressed by regulatory B cells was determined to promote B-cell-mediated immunosuppression in melanoma progression [128].…”

Section: Future Directions Of Researchmentioning

confidence: 99%

Involvement of IL-4, IL-13 and Their Receptors in Pancreatic Cancer

Shi

Song

Traub

et al. 2021

IJMS

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Interleukin (IL)-4 and IL-13 are known as pleiotropic Th2 cytokines with a wide range of biological properties and functions especially in immune responses. In addition, increasing activities have also been determined in oncogenesis and tumor progression of several malignancies. It is now generally accepted that IL-4 and IL-13 can exert effects on epithelial tumor cells through corresponding receptors. Type II IL-4 receptor (IL-4Rα/IL-13Rα1), predominantly expressed in non-hematopoietic cells, is identified to be the main target for both IL-4 and IL-13 in tumors. Moreover, IL-13 can also signal by binding to the IL-13Rα2 receptor. Structural similarity due to the use of the same receptor complex generated in response to IL-4/IL-13 results in overlapping but also distinct signaling pathways and functions. The aim of this review was to summarize knowledge about IL-4 and IL-13 and their receptors in pancreatic cancer in order understand the implication of IL-4 and IL-13 and their receptors for pancreatic tumorigenesis and progression and for developing possible new diagnostic and therapeutic targets.

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Section: Future Directions Of Researchmentioning

confidence: 99%

Involvement of IL-4, IL-13 and Their Receptors in Pancreatic Cancer

Shi

Song

Traub

et al. 2021

IJMS

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“…Hoechst 33342 dye was added at a final concentration of 7 μg/ml (231), 8 μg/ml (A549), and 10 μg/ml (HepG2) in the presence or absence of 10 μM fumitremorgin C (FTC). The following steps were described previously [8,23].…”

Section: Side Population Assaymentioning

confidence: 99%

Aspirin mediates histone methylation that inhibits inflammation-related stemness gene expression to diminish cancer stemness via COX-independent manner

Zhang

Luo

et al. 2020

Stem Cell Res Ther

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Background: The widely recognized anti-cancer potential of aspirin has created a broad interest to explore the clinical benefits of aspirin in cancer therapy. However, the current understanding of the molecular mechanisms involved in the anti-cancer potential of aspirin remains limited. Methods: Cancer stemness assays which contained ALDH, side population, chemo-resistance, sphere formation, and tumorigenesis were performed to validate aspirin function in vitro and in vivo. Histone modification assay was performed to check the effect of aspirin on histone methylation as well as the activity of HDAC and KDM6A/B. Inhibitor in vivo assay was performed to evaluate therapeutic effects of various inhibitor combination manners. Results: In regards to in vitro studies, aspirin diminishes cancer cell stemness properties which include reducing the ALDH+ subpopulation, side population, chemo-resistance, and sphere formation in three cancer types. In regards to in vivo studies, aspirin decreases tumor growth and metastasis and prolongs survival. In addition, our results showed that aspirin inhibits inflammation-related stemness gene expression (especially ICAM3) identified by a highthroughput siRNA platform. In regards to the underlying molecular mechanism of action, aspirin reduces histone demethylase (KDM6A/B) expression that mediates histone methylation and suppresses gene expression via a COXindependent manner. In regards to therapeutic strategies, aspirin combined HDM inhibitors, ICAM3 downstream signaling Src/PI3K inhibitors, or ICAM3 inhibitor Lifitigrast prevents cancer progression in vivo. Conclusions: The aforementioned findings suggest a molecular model that explains how aspirin diminishes cancer cell stemness properties. These findings may provide novel targets for therapeutic strategies involving aspirin in the prevention of cancer progression.

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“…The relationship between PPA1 expression and clinicopathological factors was examined by the Pearson χ 2 method. Two-sided P -values < 0.05 were considered statistically significant 35 .…”

Section: Methodsmentioning

confidence: 99%

PPA1 promotes NSCLC progression via a JNK- and TP53-dependent manner

et al. 2019

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Inorganic pyrophosphatase (PPA1) promotes tumor progression in several tumor types. However, the underlying mechanism remains elusive. Here, we disclosed that PPA1 expression is markedly upregulated in lung carcinoma tissue versus normal lung tissue. We also found that the non-small cell lung cancer (NSCLC) cell lines show increased PPA1 expression levels versus normal lung cell line control. Moreover, the knockdown of PPA1 promotes cell apoptosis and inhibits cell proliferation. Whereas, the ectopic expression of PPA1 reduces cell apoptosis and enhances cell proliferation. Most interestingly, the expression of mutant PPA1 (D117A) significantly abolishes PPA1-mediated effect on cell apoptosis and proliferation. The underlying mechanism demonstrated that TP53 expression deficiency or JNK inhibitor treatment could abolish PPA1-mediated NSCLC progression. In summary, the aforementioned findings in this study suggest a new pathway the PPA1 mediates NSCLC progression either via TP53 or JNK. Most important, the pyrophosphatase activity is indispensible for PPA1-mediated NSCLC progression. This may provide a promising target for NSCLC therapy.

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TBX21 predicts prognosis of patients and drives cancer stem cell maintenance via the TBX21–IL-4 pathway in lung adenocarcinoma

Cited by 21 publications

References 40 publications

Involvement of IL-4, IL-13 and Their Receptors in Pancreatic Cancer

Involvement of IL-4, IL-13 and Their Receptors in Pancreatic Cancer

Aspirin mediates histone methylation that inhibits inflammation-related stemness gene expression to diminish cancer stemness via COX-independent manner

PPA1 promotes NSCLC progression via a JNK- and TP53-dependent manner

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