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Carcinoma Invasion Pathway - Europe PMC

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Last Updated: 03 February 2022

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Enabled homolog (ENAH) regulated by RNA binding protein splicing factor 3b subunit 4 (SF3B4) exacerbates the proliferation, invasion and migration of hepatocellular carcinoma cells via Notch signaling pathway.

We wanted to determine the role of ENAH in HCC and the potential mechanism. The GEPIA2 database reported that ENAH expression in HCC tissues and the prognostic correlation. To measure ENAH expression in HCC cells, RT-qPCR and Western blot were used. The ENCORI database was designed to examine the connection between ENAH and splicing factor 3b subunit 4 in HCC tissues, which was later confirmed by RIP and actinomycin D assay. Notch1 was overexpressed to find whether ENAH affected HCC cells' biological functions by mediating Notch signaling. SF3B4 can bind to ENAH mRNA and stabilized ENAH, as well as stabilized ENAH. The influence of ENAH's ban on biological manifestations of HCC cells was reversed by Notch1 up-regulation. ENAH regulated by SF3B4 promoted the growth of HCC by inciting Notch signaling, which identified ENAH as a potent molecular target for HCC therapy and prognosis.

Source link: https://europepmc.org/article/MED/35030977


Stratifin indicates worse prognosis and promotes hepatocellular carcinoma proliferation, migration, invasion and EMT by modulating Wnt/β-catenin pathway

Methods: By western blot and RT-qPCR, protein and mRNA expression levels of SFN were identified in HCC and corresponding non-tumor tissues. SFN's prognosis value in HCC patients was determined by an online database using univariate and multivariate approach. Patients with elevated SFN levels had a poorer OS and DFS than those with poor SFN levels. SFN knockdown stimulated tumor cell proliferation, migration, invasive in vitro, and tumor formation in vivo, according to the researchers. SFN stimulated EMT and ignited the Wnt/catenin pathway, while SFN depletion reduced EMT and triggered the Wnt//catenin pathway, triggering the Wnt/>-catenin pathway. SFN results indicate poorer survival in HCC patients and encourages HCC cells' proliferation, migration, and invasion. Our findings help clarify the role and potential mechanism of SFN in HCC, providing a prognostic factor and therapeutic goal for HCC patients.

Source link: https://europepmc.org/article/PPR/PPR446476


Nogo-B promotes invasion and metastasis of nasopharyngeal carcinoma via RhoA-SRF-MRTFA pathway.

Patients with nasopharyngeal carcinoma have a poor prognosis of treatment failure. Distant metastasis remains the most common reason for treatment failure in patients with nasopharyngeal carcinoma. In vitro and in vivo, further experimental studies showed that Nogo-B overexpression could enhance the migration, and metastasis ability of NPC cells, as well as metastasis ability of NPC cells. In both NPC patients and mouse lung xenografts, a positive correlation was found between Nogo-B and the p-RhoA gene expression in NPC patients as well as in mouse lung xenografts. Nogo-B high p-RhoA high expression in N stage, M stage, and poor prognosis in NPC patients was largely associated with N stage, M stage, and poor prognosis. Notably, CCG-1423, an inhibitor of the RhoA-SRF-MRTFA pathway, may be able to reverse Nogo-B and NgR3's invasive potency in NPC cell lines and reduce the expression of N-Cadherin, suggesting that CCG-1423 might be a potential target drug of NPC. Our results reveal that Nogo-B enhances NPC cell migration and invasion potency via EMT by binding to its receptor NgR3 to regulate the RhoA-SRF-MRTFA pathway, which we summarize together.

Source link: https://europepmc.org/article/MED/35075114


ZNF488 Promotes the Invasion and Migration of Pancreatic Carcinoma Cells through the Akt/mTOR Pathway

Zin finger protein 488 is highly expressed in pancreatic carcinoma, according to published reports, but the effect on PC and its molecular mechanism remain unclear. Methods Real-time fluorescent quantitative PCR was used to detect the ZNF488 gene in PC patients' cancer tissues and cell lines. The CCK-8, cell cloning, Transwell, and scratch assays were performed to determine cell proliferation, cell cloning, migration capability, and migration ability in PANC-1 and AsPC-1 cells, respectively, after interfering with or overexpressing ZNF488 in PANC-1 and AsPC-1 cells, respectively. ZNF488 expression was clearly raised in PC tissues and cell lines, and the starBase V3. 0 database reported that the higher the ZNF488 expression, the lower the survival rate of PC patients, was evidently higher. In addition, Akt agonist SC79 could reduce the effect of the ZNF488 knockdown on Akt/mTOR pathway-related proteins, while Akt inhibitor AZD5363 had the opposite effect.

Source link: https://europepmc.org/article/MED/PMC8803468


Salvianolic acid B targets mortalin and inhibits the migration and invasion of hepatocellular carcinoma via the RECK/STAT3 pathway.

Tumor migration and invasion is a complicated and variable process that involves the epithelial-mesenchymal transition of tumor cells and the breakdown of the extracellular matrix by matrix metalloproteases, as well as matrix metalloprotease degradation. Methods Herein is a summary of the experiments carried out by the researchers. We investigated the role of mortalin in the migration of the hepatocellular carcinoma cell lines HepG2 and HCCLM3. Mortalin knockdown in HCCLM3 cells, on the other hand, raised the expression of RECK, stunted the STAT3 pathway and MMP9 production, and delayed cell migration and invasion, while humanization and invasion were reduced.

Source link: https://europepmc.org/article/MED/34876128


Transcription factor specificity protein 1-mediated Serine/threonine kinase 39 upregulation promotes the proliferation, migration, invasion and epithelial-mesenchymal transition of hepatocellular carcinoma cells by activating the transforming growth factor-β1 /Smad2/3 pathway.

This research was conducted to determine whether STK39 could be limited by specificity protein 1 to influence HCC cells' malignant processes. Firstly, STK39 expression in tissues of HCC patients and various cell lines was analyzed. Cell proliferation was examined by methyl thiazolyl tetrazolium and colony formation assay after STK39 silencing, and colony formation assay. The increased expression of STK39, which was found in both HHC patients and HCC cell lines, was observed in both HHC patients and HCC cell lines, which resulted in poor HCC prognosis. Hep3b cell proliferation, migration, invasion, EMT, TGF-1/Smad2/3 expression were inhibited by silencing, but cell apoptosis was promoted by cell apoptosis. In addition, SP1 could bind to the STK39 promoter and promote STK39 expression, which would also promote STK39 expression. Further experiments revealed that SP1 overexpression blocked the effects of STK39 silencing on Hep3b cells. HCC progression can be slowed by therapies that target SP1 to knock down STK39 expression.

Source link: https://europepmc.org/article/MED/34281492


LDLR promotes growth and invasion in renal cell carcinoma and activates the EGFR pathway.

In RCC cells with LDLR stable knockdown, the role of LDLR in RCC cell proliferation, cell cycle, and invasion was determined. The expression of LDLR expression in ccRCC tissues was higher in ccRCC tissues than in normal kidney tissues and increased with RCC progression. Following LDLR knockdown, we established an association between LDLR and EGFR, and EGFR signaling protein expression was reduced. Our results show that LDLR plays a vital role in RCC carcinogenesis, and that LDL and LDLR may be useful targets for therapeutic intervention in RCC.

Source link: https://europepmc.org/article/MED/34846158


LAGE3 promoted cell proliferation, migration, and invasion and inhibited cell apoptosis of hepatocellular carcinoma by facilitating the JNK and ERK signaling pathway.

Background Hepaticocellular carcinoma is the second leading cause of cancer death globally and lacks effective therapy due to its high incidence of tumor recurrence and metastasis. The purpose of this research was to investigate the consequences of L antigen family member 3's HCC progression. To determine the apoptosis rate of HCC cells, Annexin V-FITC/PI and TUNEL assay were used. Next, we manually controlled the expression of LAGE3 in HCC cells. The knockdown of LAGE3 slowed the proliferation of HCC cells by stopping the cell cycle in G1 phase. The downregulation of LAGE3 reduced cell migration and invasion, as well as cell death, leading to apoptosis of HCC cells, while overexpression of LAGE3 promoted the malignant phenotypes of HCC. These results were supplemented by the in vivo growth of HCC xenografts and the inhibition of apoptosis of HCC tumor cells.

Source link: https://europepmc.org/article/MED/34837962


KRT17 Facilitates Proliferation, Migration and Invasion in Esophageal Squamous Cell Carcinoma by Regulating mTOR/S6K1 pathway

Esophageal squamous cell carcinoma is one of the most common malignancies worldwide, originating from the malignant transformation of esophageal epithelial cells. Consequently, our investigation, as well as the underlying molecular mechanism of KRT17 in ESCC,MethodsData-independence acquisition-mass spectrometry workflow, was used to determine KRT17 expression between ESCC and adjacent non-cancerous esophageal tissues. The online database gene expression profiling interactive method was used to determine the difference between KRT17 expression in tissues. KRT17 in ESCC was shown to be effective on two human esophageal cancer cell lines. Cell proliferation was investigated by cell counting kit 8 reagent, colony formation assay, cell cycle replication analysis, and apoptosis. ResultsKRT17 expression was higher in cancer tissues than in normal tissues, according to Western blot and quantitative real-time PCR.

Source link: https://europepmc.org/article/PPR/PPR420627

* 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