Allicin is a safe herbal extract believed to have antitumor effects, which, however, remain unclear. The aim of the present work was to discuss Allicin antitumor effects on cervical cancer using cell experiments. Using Hela and Siha to our research objectives in our study, first step, difference concentration of Allicin (20, 40, and 80 μM) treated Hela and Siha cell lines, and next step, discuss circEIF4G2 effects in Allicin antitumor effects in Hela and Siha cell lines; the cell proliferation and EdU-positive cell number by CCK-8 and EdU staining; cell apoptosis rate by flow cytometry; invasion cell number by transwell assay; wound healing rate by wound healing assay; and relative mRNA and protein levels using qRT-PCR and WB assay. With Allicin supplement, the cell proliferation and EdU-positive cell number were significantly depressed with cell apoptosis rate significantly increasing; invasion cell number and wound healing rate significantly suppressed with circEIF4G2 mRNA expression significantly down-regulation ( < .05, respectively). However, there was no significant difference among Allicin, si-circEIF4G2, and Allicin+si-circEIF4G2 in cell biological activities including cell proliferation, apoptosis, invasion and migration, and relative gene and protein expression. Allicin depresses biological activities of cervical cancer cells through down-regulating circEIF4G2/HOXA1/AKT/mTOR.
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http://dx.doi.org/10.1002/fsn3.3935 | DOI Listing |
Elife
January 2025
Department of Diabetes and Metabolic Diseases, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Cigarette smoking is a well-known risk factor inducing the development and progression of various diseases. Nicotine (NIC) is the major constituent of cigarette smoke. However, knowledge of the mechanism underlying the NIC-regulated stem cell functions is limited.
View Article and Find Full Text PDFCancer Immunol Immunother
January 2025
Oncology Unit, Macerata Hospital, Macerata, Italy.
Introduction: Renal cell carcinoma (RCC) is one of the most common types of urogenital cancer. The introduction of immune-based combinations, including dual immune-checkpoint inhibitors (ICI) or ICI plus tyrosine kinase inhibitors (TKIs), has radically changed the treatment landscape for metastatic RCC, showing varying efficacy across different prognostic groups based on the International Metastatic RCC Database Consortium (IMDC) criteria.
Materials And Methods: This retrospective multicenter study, part of the ARON-1 project, aimed to evaluate the outcomes of favorable-risk metastatic RCC patients treated with immune-based combinations or sunitinib.
Ann Surg Oncol
January 2025
Division of Hepatobiliary and Pancreatic Surgery, Department of Surgery, The Jikei University School of Medicine, Tokyo, Japan.
Background: AT-rich interaction domain 4B (ARID4B) is a transcriptional activator that regulates the phosphatidylinositol 3-kinase (PI3K)/AKT pathway in prostate cancer. However, the role of ARID4B in hepatocellular carcinoma (HCC) has remained unclear.
Methods: This study included 162 patients who had undergone primary hepatic resection for HCC between 2008 and 2019.
Mol Genet Genomics
January 2025
Department of Botany, Biology Institute, UnB, Brasília, DF, 70910-900, Brazil.
Precursors of microRNAs (pre-miRNAs) are less used in silico to mine miRNAs. This study developed PmiR-Select based on covariance models (CMs) to identify new pre-miRNAs, detecting conserved secondary structural features across RNA sequences and eliminating the redundancy. The pipeline preceded PmiR-Select filtered 20% plant pre-miRNAs (from 38589 to 8677) from miRBase.
View Article and Find Full Text PDFNeurochem Res
January 2025
Department of Radiology, the Second Affiliated Hospital of Kunming Medical University, No.374 Yunnan-Burma Road, Wuhua District, Kunming, Yunnan, 650101, PR China.
Objective: Post-resuscitation brain injury is a common sequela after cardiac arrest (CA). Increasing sirtuin1 (SIRT1) has been involved in neuroprotection in oxygen-glucose deprivation (OGD) neurons, and we investigated its mechanism in post-cardiopulmonary resuscitation (CPR) rat brain injury by mediating p65 deacetylation modification to mediate hippocampal neuronal ferroptosis.
Methods: Sprague-Dawley rat CA/CPR model was established and treated with Ad-SIRT1 and Ad-GFP adenovirus vectors, or Erastin.
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