High ORAI3 expression correlates with good prognosis in human muscle-invasive bladder cancer

Yan, Jing; Yu, Wei; Lu, Chin‐Song; Liu, Chen; Wang, Guoliang; Jiang, Libin; Jiang, Zizheng; Qin, Zheng

doi:10.1016/j.gene.2021.145994

Cited by 4 publications

(2 citation statements)

References 73 publications

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“…As the third most common cancer worldwide, CRC develops in the setting of hereditary cancer syndromes or from infammatory bowel disease (IBD) [19], and its complex etiology involves a broad spectrum of causal factors, including environment, genetic susceptibility, and diet [4]. Whilst the mortality rate of CRC patients has been decreased due to efective cancer screening measures and multiple anticancer therapies, those patients who are not suitable for surgery or chemotherapy, or with cancer cachexia, are overlooked, and fnding a potential drug that is low-costing and efective yet of low toxicity is Accumulated investigations have demonstrated a strong regulation of cancer progression and metastasis by the reciprocal interactions between cell-intrinsic and cellextrinsic mechanisms within the TME [20,21]. In this context, targeting TME portends an ideal choice either as a monotherapy or an adjuvant in combination with other agents as well as chemotherapy.…”

Section: Discussionmentioning

confidence: 99%

Pharmacological Mechanism of Pingxiao Formula against Colorectal Cancer

Wang

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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Colorectal cancer (CRC) is the most common cancer worldwide and develops due to a broad range of causative factors. Pingxiao (PX) formula and Xihuang (XH) formula are two commonly used drugs to treat CRC, especially as an alternative therapy for those patients who could not suffer surgery, chemotherapy, or immunotherapy, namely, elder or advanced CRC patients. However, the pertinent pharmacological mechanisms are still elusive. The investigation was designed to explain the pharmacological mechanisms of the PX formula. A murine model of CRC was established by injecting CT26.WT cells into the caecum of 4-week-old male Balb/c mice, following PX or XH treatment for 30 days. Network pharmacology analysis combined with weighted gene coexpression network analysis (WGCNA) predicted the pharmacological mechanisms and therapeutic value. High-throughput 16S rRNA sequencing determined the alterations in the gut microbiota communities. Western blotting, immunofluorescence, and flow cytometry examined the influence of PX on the tumor microenvironment (TME). Injection of CT26.WT-induced CRC in Balb/c mice was markedly attenuated by PX treatment. Compared with XH administration, PX exhibited a stronger antitumor effect, such as smaller tumor volume, lower interleukin 17 (IL-17), IL-6 and tumor necrosis factor-alpha (TNFα) serum levels, and higher interferon-gamma (IFN-γ) concentration. Network pharmacology analysis demonstrated that both PX and XH targets were enriched in cancers and inflammatory responses. RNA sequencing confirmed that PX treatment induced cancer cell apoptosis and inhibited inflammatory reactions within the tumor. Moreover, the PX formula considerably restored homeostasis of the gut microbiota, which was not observed in the XH group. PX targets, those associated with the survival probability of CRC patients, correlated with macrophage (Mφ) infiltration, which presented an independent risk factor for the CRC outcome. PX treatment promoted the transition of alternatively activated Mφs (M2 Mφs) to classically activated Mφs (M1 Mφs). Moreover, the peritoneal Mφs from the PX group inhibited the migration of CW26.WT cells, as evidenced by the wound healing experiment and transwell assay, which was consistent with the decreased expression of the vascular endothelial growth factor (VEGF). Furthermore, the coculturing system confirmed that PX-treated Mφs suppressed colorectal tumor-derived organoid proliferation. PX formula exhibits a potential antitumor effect against CRC by suppressing the colonization of pathological microorganisms, reshaping Mφ effector functions and hence inhibiting cancer cell proliferation.

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Section: Discussionmentioning

confidence: 99%

Pharmacological Mechanism of Pingxiao Formula against Colorectal Cancer

Wang

et al. 2022

Evidence-Based Complementary and Alternative Medicine

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“…Tumor cell-secreted CCL20 and CCL22 in the pleural effusion act on the corresponding receptors CCR4 and CCR6 on Th17 cells and recruit them ( 117 ). Additionally, in invasive bladder cancer, the recruitment of Th17 cells through chemokines is involved in exerting antitumor effects ( 118 ). These findings suggest that directly recruited Th17 cells can play an antitumor role within the tumor microenvironment.…”

Section: The Signaling Molecules Contributing To Th17 Cells In the Tu...mentioning

confidence: 99%

Factors impacting the benefits and pathogenicity of Th17 cells in the tumor microenvironment

Xing,

Man,

Liu

et al. 2023

Front. Immunol.

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Tumor development is closely associated with a complex tumor microenvironment, which is composed of tumor cells, blood vessels, tumor stromal cells, infiltrating immune cells, and associated effector molecules. T helper type 17 (Th17) cells, which are a subset of CD4+ T cells and are renowned for their ability to combat bacterial and fungal infections and mediate inflammatory responses, exhibit context-dependent effector functions. Within the tumor microenvironment, different molecular signals regulate the proliferation, differentiation, metabolic reprogramming, and phenotypic conversion of Th17 cells. Consequently, Th17 cells exert dual effects on tumor progression and can promote or inhibit tumor growth. This review aimed to investigate the impact of various alterations in the tumor microenvironment on the antitumor and protumor effects of Th17 cells to provide valuable clues for the exploration of additional tumor immunotherapy strategies.

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