RAF1 (c‐raf) has been known as an important tumor‐promoter in many cancers. However, the regulatory mechanisms affecting RAF1 expressions are rarely reported. This study aimed to predict the candidate miRNAs of RAF1 gene and verify their functions in the progression of lung cancer. The expression of miR‐643 was detected by reverse transcription polymerase chain reaction (RT‐PCR). A dual‐luciferase report system was used to verify the relationship between miR‐643 and RAF1. RT‐PCR and Western blot were used to analyze the regulatory relationship between miR‐643 and RAF1. Transwell chamber, scratch, and monoclonal tests showed that miR‐643 affected the proliferation, migration, and radiosensitivity of H1299 and A549 cells by targeting the RAF1 gene. The expression of miR‐643 in lung cancer cells was lower than that in the bronchial epithelioid cells (CRL‐2741), and luciferase reporter experiment confirmed that miR‐643 targeted RAF1. MiR‐643 overexpression decreased the RAF1 expression, thereby decreasing cell migration, proliferation, and radiation resistance through the AKT/nuclear factor‐κB pathway. miR‐643 in lung cancer cells could inhibit cell proliferation, invasion, and metastasis and increase the radiosensitivity by downregulating RAF1.
Hypocalcemia is a fatal electrolytic disorder defined as corrected serum total calcium levels <2.12 mmol/L (8.5 mg/dl). Drug-induced hypocalcemia is uncommon. A female patient was admitted to Jiangsu Cancer Hospital and diagnosed with nasopharyngeal carcinoma; she developed hypocalcemia after chemotherapy with albumin-bound paclitaxel. Its diagnosis is incredibly difficult. Confirmatory diagnosis depends on serum total calcium levels and electrocardiogram.
Background: Acyl-coenzyme A cholesterol acyltransferase (ACAT) is a membrane-binding enzyme, which localizes in the endoplasmic reticulum. ACAT2 can promote the progression of colon cancer, but its efficacy in lung adenocarcinoma(LUAD) is still not sure. Method: ACAT2 expression analysis was performed by TIMER2.0 database. GEPIA database was utilized to analyse co-relations between expression of ACAT2 and pathological stage of tumor. Kaplan-Meier analysis was analyzed its potential in clinical prognosis. CancerSEA database analysed correlations between expression of ACAT2 and functional status of different tumor displayed as a heatmap. The molecule interaction network analysis performed by the STRING tool. Results: ACAT2 was upregulated in patients with LUAD, and high expression of ACAT2 had a poor DFS and OS. Cox regression analysis indicated that the poor outcomes might be related to the tumour stage, nodal stage, distant metastatic stage. ACAT2 participated in biological process of cell cycle, DNA repair, DNA damage, proliferation. Enrichment pathway analysis showed four ACAT2-correlated genes, ACOX1, EHHADH, OXCT1, DLAT. Conclusion: ACAT2 might be a novel predictive biomarker and treated target.
Background: Acyl-coenzyme A cholesterol acyltransferase (ACAT) is a membrane-binding enzyme, which localizes in the endoplasmic reticulum. ACAT2 can promote the progression of colon cancer, but its efficacy in lung adenocarcinoma(LUAD) remains uncertain. Method: Analysis of ACAT2 expression was performed using TIMER2.0 database. The GEPIA database was utilized to analyze the correlation between ACAT2 expression and pathological stage of the tumour. The Kaplan-Meier analysis was performed to analyze its potential in clinical prognosis. The correlation between expression of ACAT2 and functional status of different tumours was analyzed in the CancerSEA database and displayed as a heatmap. Molecular interaction network analysis performed with the STRING tool. Results: High ACAT2 expression was associated with a poor DFS and OS in LUAD patients. Cox regression analysis indicated that the poor outcomes might be related to tumour stage, nodal stage, distant metastatic stage. ACAT2 was involved in many biological processes including the cell cycle, DNA repair, DNA damage, and proliferation. Enrichment pathway analysis revealed four ACAT2 related genes, ACOX1, EHHADH, OXCT1, DLAT.
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