TBX21 attenuates colorectal cancer progression via an ARHGAP29/RSK/GSK3β dependent manner

Jiang, Xinyu; Du, Wenfei; Yang, Chenglong; Wang, Shuying; Li, Yifei; Shen, Xinzhuang; Yang, Xiaowen; Yao, Jie; Du, Renle; Zhang, Xiaoyuan; Huang, Yingqi; Shen, Wenzhi

doi:10.1007/s13402-023-00809-6

Cited by 4 publications

(1 citation statement)

References 30 publications

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“…Decreased expression RSK1 Lung adenocarcinomas [14] , Leukemia [20] , CRC [21] , Renal cancer [22] , Ovarian cancer [23] , Glioma [24] Breast cancer [25] RSK2 Glioma [24] , Breast cancer [25,26] , Lung cancer [27] , Leukemia [28] , Ovarian cancer [29] CRC [30] RSK3 -Breast cancer [25] , Lung cancer [31] , Ovarian cancer [32] RSK4 Renal cancer [33] , Glioma [34,35] Breast cancer [36] , Lung cancer [37] , CRC [38] , Leukemia [39] , Esophageal cancer [40] , Ovarian cancer [41] CRC: Colorectal cancer. dependent manner [42] .…”

Section: Increased Expressionmentioning

confidence: 99%

Regulation and function of the RSK family in colorectal cancer

Wang,

Han,

Lei

et al. 2024

J Cancer Metastasis Treat

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P90 Ribosomal S6 Kinases (RSKs) constitute a class of Serine/Threonine (Ser/Thr) protein kinases and play a critical role as downstream targets in the Raf/MEK/ERK signaling pathway. Gaining insight into the biological function of RSK family proteins, given their functions in various tumors, is vital. The RSK family is involved in the regulation of cellular functions including cell proliferation, motility, invasion, and survival. The RSK family comprises four human isoforms (RSK1, RSK2, RSK3, and RSK4). The activation of RSK protein kinases is mediated through direct phosphorylation by extracellular signal-regulated kinase 1/2 (ERK1/2) and phosphoinositide-dependent kinase 1 (PDK1) after the Ras/MAPK (mitogen-activated protein kinase) pathway is activated. Recent evidence suggests that RSK family proteins promote the onset and metastasis of cancer, leading to the association of the protein expression of these kinases with various cancer types, such as colorectal cancer (CRC), breast cancer, lung cancer, kidney cancer, leukemia, esophageal squamous cell carcinoma, ovarian cancer, glioma, and endometrial cancer. In this review, we summarize the latest research on the RSK family, focusing on its role in patients with CRC, along with associated treatment challenges and limitations. This information enhances our comprehension of the regulation and function of RSK family proteins, highlighting their potential as both clinical biomarkers for diagnosing CRC and targets for molecular therapeutic interventions in the future.

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Section: Increased Expressionmentioning

confidence: 99%

Regulation and function of the RSK family in colorectal cancer

Wang,

Han,

Lei

et al. 2024

J Cancer Metastasis Treat

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A comprehensive view on the fisetin impact on colorectal cancer in animal models: Focusing on cellular and molecular mechanisms

Zamanian,

Taheri,

Ramadan

et al. 2024

Anim Models and Exp Med

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Flavonoids, including fisetin, have been linked to a reduced risk of colorectal cancer (CRC) and have potential therapeutic applications for the condition. Fisetin, a natural flavonoid found in various fruits and vegetables, has shown promise in managing CRC due to its diverse biological activities. It has been found to influence key cell signaling pathways related to inflammation, angiogenesis, apoptosis, and transcription factors. The results of this study demonstrate that fisetin induces colon cancer cell apoptosis through multiple mechanisms. It impacts the p53 pathway, leading to increased levels of p53 and decreased levels of murine double minute 2, contributing to apoptosis induction. Fisetin also triggers the release of important components in the apoptotic process, such as second mitochondria‐derived activator of caspase/direct inhibitor of apoptosis‐binding protein with low pI and cytochrome c. Furthermore, fisetin inhibits the cyclooxygenase‐2 and wingless‐related integration site (Wnt)/epidermal growth factor receptor/nuclear factor kappa B signaling pathways, reducing Wnt target gene expression and hindering colony formation. It achieves this by regulating the activities of cyclin‐dependent kinase 2 and cyclin‐dependent kinase 4, reducing retinoblastoma protein phosphorylation, decreasing cyclin E levels, and increasing p21 levels, ultimately influencing E2 promoter binding factor 1 and cell division cycle 2 (CDC2) protein levels. Additionally, fisetin exhibits various effects on CRC cells, including inhibiting the phosphorylation of Y‐box binding protein 1 and ribosomal S6 kinase, promoting the phosphorylation of extracellular signal‐regulated kinase 1/2, and disrupting the repair process of DNA double‐strand breaks. Moreover, fisetin serves as an adjunct therapy for the prevention and treatment of phosphatidylinositol‐4,5‐bisphosphate 3‐kinase catalytic subunit α (PIK3CA)‐mutant CRC, resulting in a reduction in phosphatidylinositol‐3 kinase (PI3K) expression, Ak strain transforming phosphorylation, mTOR activity, and downstream target proteins in CRC cells with a PIK3CA mutation. These findings highlight the multifaceted potential of fisetin in managing CRC and position it as a promising candidate for future therapy development.

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