Examination of the effects of capecitabine treatment on the HT-29 colorectal cancer cell line and HCG 11, HCG 15, and HCG 18 lncRNAs in CRC patients before and after chemotherapy

Colorectal cancer (CRC) is the third most common malignancy worldwide. Long noncoding RNAs (lncRNAs) are involved in several pathogenic pathways related to CRC. This study aimed to compare the expression profiles of HCG11, HCG15, and HCG18 genes in CRC patients before and after chemotherapy. Moreove...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Naunyn-Schmiedeberg's archives of pharmacology 2024-12
Hauptverfasser: Alkharsan, Abdulrasool M Hussein M S, Safaralizadeh, Reza, Khalaj-Kondori, Mohammad, HosseinpourFeizi, Mohammadali
Format: Artikel
Sprache:eng
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
Beschreibung
Zusammenfassung:Colorectal cancer (CRC) is the third most common malignancy worldwide. Long noncoding RNAs (lncRNAs) are involved in several pathogenic pathways related to CRC. This study aimed to compare the expression profiles of HCG11, HCG15, and HCG18 genes in CRC patients before and after chemotherapy. Moreover, capecitabine's effects, which is a chemotherapeutic agent, were investigated on apoptosis, cell cycle, and the lncRNA expression in CRC using HT-29 cells. qRT-PCR was used to measure lncRNAs expression in patient and healthy tissues, and the HT-29 CRC cell line. Additionally, the diagnostic and prognostic utility of these lncRNAs were assessed using the ROC curve analysis. The MTT assay was used to evaluate the cytotoxicity of capecitabine, and by using flow cytometry, apoptosis induction and cell cycle progression were investigated. CRC patients expressed higher levels of HCG11 and HCG15 and lower levels of HCG18. Furthermore, those receiving capecitabine demonstrated a decrease in HCG11 and an increase in HCG18 expression. In the HT-29 cell line, capecitabine can also increase the expression of HCG18 and decrease the expression of HCG11 and HCG15. However, no statistically significant variations were determined in the expression of these lncRNAs in clinical variables. Additionally, the data show that HCG18 is a poor prognostic biomarker, and HCG11 and HCG18 are poor diagnostic biomarkers. Treatment with capecitabine caused an accumulation of sub-G1 cells, indicating a potent apoptotic effect on HT-29 cells. These findings confirmed capecitabine's anticancer effects and showed that it can increase HCG18 and reduce HCG11 and HCG15 expression.
ISSN:1432-1912
1432-1912
DOI:10.1007/s00210-024-03674-8