Ionizing radiation is genotoxic to the cell, and p53 is commonly considered to be a key regulator that controls gene expression responding to the genotoxity of radiation. The expression profiles of microRNAs (miRNAs), which are small non-coding RNAs regulating the translation of target mRNAs, were analyzed to determine whether any correlation exists between miRNA expression, radiation response, and/or p53. The miRNA profiles were analyzed by microarray containing 470 human miRNA probes in HCT116 human colon carcinoma cells and their p53-null derivative. Thirty-eight miRNAs among the 138 flagged human miRNAs were selected by fold-change analysis. The expression levels of these 38 miRNAs were changed more than two-fold, and a total of 12 miRNAs were significantly affected by p53, radiation, and the combination of both. All 12 miRNAs had expression patterns correlated to p53, while two miRNAs were affected by radiation or the combined action of radiation and p53. In bioinformatics studies, these miRNAs had p53-binding sites with scores higher than 85% in their upstream regions, and some of their target genes were found to be involved in genotoxic responses. In conclusion, we have identified miRNAs influenced significantly by p53 and/or radiation in the HCT116 human colon carcinoma cell line model, and these miRNAs may have important roles in the regulation of genes involved the cellular responses to radiation.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.3892/ijo_00000295 | DOI Listing |
Curr Issues Mol Biol
December 2024
Department of Regenerative Medicine, School of Pharmaceutical Sciences, Jilin University, Changchun 130021, China.
Lymphocyte antigen 6 complex, locus K (LY6K) is a putative oncogene in various human cancers, including colorectal cancer, where elevated expression is associated with poor prognosis. This study investigates the antitumor effects of LY6K in colon cancer stem cells (CCSCs) both in vitro and in vivo. EpCAM and CD44 surface markers were used to isolate CCSCs from HCT116 cells, and the expression of LY6K in CCSCs was analyzed by real-time PCR.
View Article and Find Full Text PDFJ Cancer Res Clin Oncol
December 2024
Zhuhai Tengbai Pharmaceutical Co., Ltd, Zhuhai, 519031, China.
Background: Colorectal cancer (CRC) is the third most common cancer globally, with advanced stages presenting significant treatment challenges. Recently years, drug combination therapy has become a promising strategy for cancer treatment.
Objective: To evaluate the therapeutic efficacy of the combination of the anti-angiogenic drug PEP06 (TB01) and the cytotoxic drug Trifluridine/Tipiracil (TAS-102) in human CRC HCT-116 xenograft mouse model.
Se Pu
January 2025
School of Marine Sciences, Sun Yat-sen University, Zhuhai 519082, China.
Oncol Rep
February 2025
Department of Gastroenterological Surgery, Nagoya City University Graduate School of Medical Sciences, Nagoya, Aichi 467‑8601, Japan.
BH3 mimetics are small‑molecule inhibitors of the antiapoptotic Bcl‑2 family and have therapeutic efficacy against hematological malignancies. BH3 mimetic A‑1331852 suppresses colorectal cancer cell proliferation. Progressive resistance to the widely used anticancer agent fluorouracil (5‑FU) is a key reason for colorectal cancer recurrence; therefore, the present study tested if A‑1331852 can suppress the proliferation of 5‑FU‑resistant colorectal cancer cells.
View Article and Find Full Text PDFDrug Dev Res
February 2025
Department of Pharmaceutical Organic Chemistry, Faculty of Pharmacy, Mansoura University, Mansoura, Egypt.
Five series of new 1,3,4-thiadiazole hybrids were designed and synthesized as promising EGFR inhibitors. Three human cancer cell lines were employed for testing each hybrid's in vitro antiproliferative efficacy; colon HCT-116, liver HepG-2 and breast MCF-7 using MTT assay. Comparing compound 9a to the reference doxorubicin, 9a shown superior activity to that of Dox with respect to MCF-7 (IC 3.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!