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AKT ERK Signaling - Europe PMC

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Last Updated: 15 February 2022

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The Protective Role of Celastrol in Renal Ischemia-Reperfusion Injury by Activating Nrf2/HO-1, PI3K/AKT Signaling Pathways, Modulating NF-κb Signaling Pathways, and Inhibiting ERK Phosphorylation.

In a kidney ischemia-reperfusion injury rat model, we investigated celastrol's antioxidant activity by testing calcium oxide 3-kinase B2 /heme oxygenase B signaling, nuclear factor-kappa B pathways, and extracellular signal-regulated kinase 2-related factor 2 /heme oxygenase B pathways. Rats were given celastrol 2 mg/kg orally for 1 week before subjection to renal ischemia-reperfusion surgery. Pretreatment of Celastrol attenuated oxidative stress, increased Nrf2 gene expression, and HO-1 levels, as well as increased HO-1 levels.

Source link: https://europepmc.org/article/MED/35157199


CircCCNB1 silencing acting as a miR-106b-5p sponge inhibited GPM6A expression to promote HCC progression by enhancing DYNC1I1 expression and activating the AKT/ERK signaling pathway.

However, no studies have been published on the role of a circRNA-based competitive endogenous RNA network in hepatocellular carcinoma, however, few research has been done. The ceRNA networks were built using Cytoscape tools, based on two models of up-regulated circRNA/down-regulated mRNA/down-regulated miRNA/up-regulated miRNA/down-regulated mRNA and down-regulated miRNA/down-regulated mRNA and down-regulated miRNA/down-regulated mRNA/down-regulated miRNA/down-regulated miRNA/regulated miRNA/down-regulated mRNA/down-regulated miRNA/down-regulated miRNA For determining the RNA expression levels in HCC cells and tissues, the qRT-PCR technique was used. HCC cell proliferation in vitro and in vivo was investigated by hsa_circ_0001495 silencing and overexpression. The following results: Twenty DE-circRNAs with a genome length less than 2000bp, 11 survival-related DE-mRNAs, and 61 survival-related DE-mRNAs were tested out and used to create five HCC-related ceRNA networks. HCC cells and tumor tissues were significantly down-regulated by circCCNB1 and GPM6A expression, while miR-106b-5p was up-regulated. Following transfections, miR-106b-5p mimics greatly enhanced HCC cell proliferation, migration, and metastasis, according to miR-105b-5p inhibitor, although the reverse was seen with miR-105b-5p inhibitor. In addition, circulation-based silencing increased the clone generation capability, the cell cycle G1-S transition, and the development of xenograft tumors of HCC cells via GPM6A downregulation. GPM6A deficient cell line regulation was stimulated by the expression of DYNC1I1I1I1 and stimulated the AKT/ERK pathway to regulate the HCC cell cycle. Conclusions: We showed that circconned silencing promoted cell proliferation and metastasis of HCC cells by weakening sponging of oncogenic miR-106b-5p to produce GPM6A underexpression.

Source link: https://europepmc.org/article/MED/35002514


Harmine Hydrochloride Triggers G2/M Cell Cycle Arrest and Apoptosis in HCT116 Cells through ERK and PI3K/AKT/mTOR Signaling Pathways.

Colorectal carcinoma is one of the most common and aggressive malignant carcinomas. In this research, we investigated the anticancer effects of harmine hydrochloride, a hydrophilic and stable drug that is easily absorbed by tissues and similar to harmine, as well as the underlying mechanism of action in human CRC HCT116 cells. HMH also induced G2 cell cycle arrest by lowering the expression of p-cdc2, cdc2, and cyclin B1, proteins that control the G2/M phase, as well as the expression of Rb, a protein that regulates cell proliferation in a dose-dependent manner. Also, HMH reduced the amount of p-ERK, p-PI3K, p-AKT, and p-mTOR in HCT116 cells, dramatically inhibiting p-ERK and p-AKT expression in cells treated with hMH and PD98059, an AKT inhibitor, or LY294002, an AKT inhibitor.

Source link: https://europepmc.org/article/MED/35047441


Ursolic Acid Decreases the Proliferation of MCF-7 Cell-Derived Breast Cancer Stem-Like Cells by Modulating the ERK and PI3K/AKT Signaling Pathways.

The cancer stem cells in tumors and cancer relapse are both common sources of metastasis and cancer relapse, making them important therapeutic targets. Ursolic acid, a pentacyclic triterpenoid, has anticancer effects in a variety of cancers; however, little is known about its effect on MCF-7 cell-derived breast cancer stem -like cells in estrogen receptor positive breast cancer stem -like cells. UA raised p53 and p21 expression in MCF-7 cells, but decreased cyclin D, CDK4, and CDK2 expression to induce cell cycle arrest in the G0/G1 phase.

Source link: https://europepmc.org/article/MED/35047440


Inhibition of glioblastoma progression by Urolithin A in vitro and in vivo by regulating Sirt1-FOXO1 axis via ERK/AKT signaling pathways.

On UA incubation, flow cytometry was used to determine cell cycle arrest and apoptosis of U251 and U118 MG cells. Moreover, UA could raise the expression levels of Sirt1 and FOXO1 and FOXO1 in conjunction with Sirt1 and FOXO1 and FOXO1's deposition and migration of glioblastoma cells, as well as Sirt1 and FOXO1, and Sirt1's demise of Sirt1 and FOXO1 and FOXO1 and FOXO1; also, Sirt1 and FOXO1 and FOXO1 and UA'sy UA reduced the tumor size and weight of glioblastoma in xenograft nude mice and boosted the expression of Sirt1 and FOXO1 in transplanted tumors in animal experiments. According to our results, UA exerts a repressive action on glioblastoma cells both in vivo and in vitro by governing the Sirt1-FOXO1 axis via the ERK and AKT pathways, indicating that UA is a new novel therapeutic candidate for the treatment of glioblastoma.

Source link: https://europepmc.org/article/MED/34818027


Cinnamomi Ramulus Inhibits the Growth of Colon Cancer Cells Via Akt/ERK Signaling Pathways

Background: Colon cancer is the second highest mortality rate among malignant tumors worldwide, and current conventional therapy regimens are not very effective. The unique efficacy of Chinese herb medicine for cancer has recently drew increasing interest. Methods of TCMSP and China National Knowledge Infrastructure database were used to forecast the candidate ingredients of CR, and the TCMSP and SwissTargetPrediction database were also used to forecast the drug targets of the candidate ingredients from CR. Oral administration of CR in C57BL/6 mice could stifle CC cells, which may also reduce the viability and motility of CC cells. Meanwhile, we found 111 potential therapeutic targets in CC cells, as well as enrichment studies showed that CR could cause apoptosis and cell cycle arrest in CC cells by blocking the Akt/ERK signaling pathways.

Source link: https://europepmc.org/article/PPR/PPR424485

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions

* Please keep in mind that all text is summarized by machine, we do not bear any responsibility, and you should always check original source before taking any actions