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RIPK4 driven by TP53 mutations promotes resistance to PANoptosis and metastasis of CRC by phosphorylation of MTHFD1

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE252264 | GEO | 2025/02/01

REPOSITORIES: GEO

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RIPK4 driven by TP53 mutations promotes resistance to PANoptosis and metastasis of CRC by phosphorylation of MTHFD1 [RIPK4_sh_seq]

Project description:In this study, we found that RIPK4 protein driven by TP53 mutation is highly expressed in CRC, which can promote the phosphorylation level of MTHFD1 (Methylenetetrahydrofolate Dehydrogenase, Cyclohydrolase And Formyltetrahydrofolate Synthetase 1), a key enzyme of carbon metabolism, promote the generation of NADPH in CRC cells, and reduce the level of ROS, thus promoting PANoptosis resistance and distant metastasis of CRC cells. We explain the novel mechanism of metastasis induced by the TP53 mutation in terms of post-translational modification and clarify the biological role of the RIPK4 protein in CRC, which can be used as a new target for the treatment of metastatic CRC.

2025-02-01 | GSE252263 | GEO

RIPK4 driven by TP53 mutations promotes resistance to PANoptosis and metastasis of CRC by phosphorylation of MTHFD1 [Anokis_seq]

2025-02-01 | GSE252262 | GEO

RIPK4 driven by TP53 mutations promotes resistance to PANoptosis and metastasis of CRC by phosphorylation of MTHFD1

Project description:Changes in intracellular proteins of CRC cells in a suspended state

2023-12-07 | PXD047592 |

RIPK4 driven by TP53 mutations promotes resistance to PANoptosis and metastasis of CRC by phosphorylation of MTHFD1

Project description:RIPK4 driven by TP53 mutations promotes resistance to PANoptosis and metastasis of CRC by phosphorylation of MTHFD1

| PRJNA1059024 | ENA

RIPK4 driven by TP53 mutations promotes resistance to PANoptosis and metastasis of CRC by phosphorylation of MTHFD1 [RIPK4_sh_seq]

Project description:RIPK4 driven by TP53 mutations promotes resistance to PANoptosis and metastasis of CRC by phosphorylation of MTHFD1 [RIPK4_sh_seq]

| PRJNA1059031 | ENA

RIPK4 driven by TP53 mutations promotes resistance to PANoptosis and metastasis of CRC by phosphorylation of MTHFD1 [Anokis_seq]

Project description:RIPK4 driven by TP53 mutations promotes resistance to PANoptosis and metastasis of CRC by phosphorylation of MTHFD1 [Anokis_seq]

| PRJNA1059030 | ENA

RIPK4 Suppresses the Invasion and Metastasis of Hepatocellular Carcinoma by Inhibiting the Phosphorylation of STAT3.

Project description:Receptor interacting serine/threonine kinase 4 (RIPK4) is a member of the threonine/serine protein kinase family; it plays related functions in a variety of tumours, but its biological function has not been fully revealed. It has been reported that it is differentially expressed in hepatocellular carcinoma (HCC). Our research aimed to reveal the role of RIPK4 in the progression of HCC and to reveal the biological behaviour of RIPK4 in HCC. We analysed the differences in RIPK4 expression in HCC by using a publicly available data set. By using PCR, Western blotting and immunohistochemical staining methods, we detected the expression level of RIPK4 in HCC patient specimens and studied the relationship between the expression of RIPK4 and the clinicopathological features of HCC patients. The prognostic data were combined to analyse the relationship between RIPK4 and HCC patient survival and tumour recurrence. We found that the expression level of RIPK4 in nontumour tissues was significantly higher than that in tumour tissues, and the level of RIPK4 was significantly positively correlated with postoperative survival and recurrence in HCC patients. Further, our study found that RIPK4 inhibits the progression of HCC by influencing the invasion and metastasis of HCC and that overexpression of RIPK4 reduces the invasion and metastasis of HCC by inhibiting epithelial-mesenchymal transition (EMT) and the STAT3 pathway. In in vivo experiments, overexpression of RIPK4 stably inhibited HCC metastasis. To summarize, our research revealed the relationship between RIPK4 and the prognosis of patients with HCC. We discovered that RIPK4 affects the invasion and metastasis of HCC through the EMT and STAT3 pathways. Targeted inhibition of the RIPK4 gene and the STAT3 pathway may be potential therapeutic strategies for inhibiting the postoperative recurrence and metastasis of HCC.

| S-EPMC8249771 | biostudies-literature

Phosphorylation of Dishevelled by protein kinase RIPK4 regulates Wnt signaling.

Project description:Receptor-interacting protein kinase 4 (RIPK4) is required for epidermal differentiation and is mutated in Bartsocas-Papas syndrome. RIPK4 binds to protein kinase C, but its signaling mechanisms are largely unknown. Ectopic RIPK4, but not catalytically inactive or Bartsocas-Papas RIPK4 mutants, induced accumulation of cytosolic β-catenin and a transcriptional program similar to that caused by Wnt3a. In Xenopus embryos, Ripk4 synergized with coexpressed Xwnt8, whereas Ripk4 morpholinos or catalytic inactive Ripk4 antagonized Wnt signaling. RIPK4 interacted constitutively with the adaptor protein DVL2 and, after Wnt3a stimulation, with the co-receptor LRP6. Phosphorylation of DVL2 by RIPK4 favored canonical Wnt signaling. Wnt-dependent growth of xenografted human tumor cells was suppressed by RIPK4 knockdown, suggesting that RIPK4 overexpression may contribute to the growth of certain tumor types.

| S-EPMC4094295 | biostudies-literature

Phosphorylation of Pkp1 by RIPK4 regulates epidermal differentiation and skin tumorigenesis.

Project description:Tissue homeostasis of skin is sustained by epidermal progenitor cells localized within the basal layer of the skin epithelium. Post-translational modification of the proteome, such as protein phosphorylation, plays a fundamental role in the regulation of stemness and differentiation of somatic stem cells. However, it remains unclear how phosphoproteomic changes occur and contribute to epidermal differentiation. In this study, we survey the epidermal cell differentiation in a systematic manner by combining quantitative phosphoproteomics with mammalian kinome cDNA library screen. This approach identified a key signaling event, phosphorylation of a desmosome component, PKP1 (plakophilin-1) by RIPK4 (receptor-interacting serine-threonine kinase 4) during epidermal differentiation. With genome-editing and mouse genetics approach, we show that loss of function of either Pkp1 or Ripk4 impairs skin differentiation and enhances epidermal carcinogenesis in vivo Phosphorylation of PKP1's N-terminal domain by RIPK4 is essential for their role in epidermal differentiation. Taken together, our study presents a global view of phosphoproteomic changes that occur during epidermal differentiation, and identifies RIPK-PKP1 signaling as novel axis involved in skin stratification and tumorigenesis.

| S-EPMC5494465 | biostudies-literature

TP53 Mutations as a Driver of Metastasis Signaling in Advanced Cancer Patients.

Project description:Molecular profiling with next generation sequencing (NGS) delivers key information on mutant gene sequences, copy number alterations, gene-fusions, and with immunohistochemistry (IHC), is a valuable tool in clinical decision making for patients entering investigational agent trials. Our objective was to elucidate mutational profiles from primary versus metastatic sites from advanced cancer patients to guide rational therapy. All phase I patients (n = 203) with advanced cancer were profiled by commercially available NGS platforms. The samples were annotated by histology, primary and metastatic site, biopsy site, gene mutations, mutation count/gene, and mutant TP53. A molecular profile of each patient was categorized into common and unique mutations, signaling pathways for each profile and TP53 mutations mapped to 3D-structure of p53 bound to DNA and pre/post therapy molecular response. Of the 171 patients analyzed, 145 had genetic alterations from primary and metastatic sites. The predominant histology was adenocarcinoma followed by squamous cell carcinoma, carcinoma of unknown primary site (CUPS), and melanoma. Of 790 unique mutations, TP53 is the most common followed by APC, KRAS, PIK3CA, ATM, PTEN, NOTCH1, BRCA2, BRAF, KMT2D, LRP1B, and CDKN2A. TP53 was found in most metastatic sites and appears to be a key driver of acquired drug resistance. We highlight examples of acquired mutational profiles pre-/post- targeted therapy in multiple tumor types with a menu of potential targeted agents. Conclusion: The mutational profiling of primary and metastatic lesions in cancer patients provides an opportunity to identify TP53 driver 'pathways' that may predict for drug sensitivity/resistance and guide rational drug combinations in clinical trials.

| S-EPMC7913278 | biostudies-literature

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