International Journal of Molecular and Cellular Medicine (IJMCM)
Cellular and Molecular Biology Research Center, Babol University of Medical Sciences
شنبه 12 مهر 1404
[Archive]
جلد 0 -
|
برگشت به فهرست نسخه ها
Download citation:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
BibTeX | RIS | EndNote | Medlars | ProCite | Reference Manager | RefWorks
Send citation to:
Alighardashi Z, Moradzad M, Najafpour S, Vahabzadeh Z. Evidence for a TMAO-HULC-miRNA regulatory axis in colorectal cancer cells. Int J Mol Cell Med 2025;
URL: http://ijmcmed.org/article-1-2608-fa.html
URL: http://ijmcmed.org/article-1-2608-fa.html
Evidence for a TMAO-HULC-miRNA regulatory axis in colorectal cancer cells. مجله بین المللی سلولی و مولکولی. 1404;
: (4 مشاهده)
Colorectal cancer (CRC) is a malignancy with a significant global disease burden.Trimethylamine N-oxide (TMAO), a gut microbiota-derived metabolite, has been implicated in tumorigenesis. The oncogenic long non-coding RNA highly upregulated in liver cancer (HULC) plays a pivotal role in CRC progression. However, the exact molecular mechanism of HULC and its correlation with TMAO in CRC pathogenesis has remained unclear. This study tested whether TMAO regulates HULC and whether HULC mediates changes in selected miRNAs relevant to CRC.
Caco-2 cells were treated with TMAO (300 µM, 24 h) and HULC expression was quantified by RT-qPCR. HULC was transiently silenced using CRISPR/Cas13 (CasRx) and the expression of candidate downstream miRNAs (miR-21-5p, miR-200a-3p and miR-34a-5p) was measured by stem-loop RT-qPCR. Data are presented as mean ± SD of at least three independent biological replicates. Group differences were analyzed by ANOVA with appropriate post-hoc testing.
TMAO treatment significantly increased HULC expression in Caco-2 cells. TMAO also elevated miR-21-5p and miR-200a-3p levels; these increases were attenuated when HULC was silenced. miR-34a-5p expression was not significantly affected by TMAO or by HULC knockdown.
This study demonstrates that TMAO upregulates the oncogenic lncRNA HULC, and this upregulation is associated with increases the expression of miR-21-5p and miR-200a-3p. These findings reveal a TMAO-HULC signaling axis that positively influences the levels of oncogenic miRNAs. However, since a single cell line model was used in this study, it needs for further investigation across diverse CRC cell lines to confirm its generalizability.
Caco-2 cells were treated with TMAO (300 µM, 24 h) and HULC expression was quantified by RT-qPCR. HULC was transiently silenced using CRISPR/Cas13 (CasRx) and the expression of candidate downstream miRNAs (miR-21-5p, miR-200a-3p and miR-34a-5p) was measured by stem-loop RT-qPCR. Data are presented as mean ± SD of at least three independent biological replicates. Group differences were analyzed by ANOVA with appropriate post-hoc testing.
TMAO treatment significantly increased HULC expression in Caco-2 cells. TMAO also elevated miR-21-5p and miR-200a-3p levels; these increases were attenuated when HULC was silenced. miR-34a-5p expression was not significantly affected by TMAO or by HULC knockdown.
This study demonstrates that TMAO upregulates the oncogenic lncRNA HULC, and this upregulation is associated with increases the expression of miR-21-5p and miR-200a-3p. These findings reveal a TMAO-HULC signaling axis that positively influences the levels of oncogenic miRNAs. However, since a single cell line model was used in this study, it needs for further investigation across diverse CRC cell lines to confirm its generalizability.
نوع مطالعه: Original Article |
موضوع مقاله:
Cell Biology
دریافت: 1404/3/11 | پذیرش: 1404/6/12 | انتشار: 1404/5/6
دریافت: 1404/3/11 | پذیرش: 1404/6/12 | انتشار: 1404/5/6
Supplementary 1 [PDF 386 KB] (1 دریافت)
| بازنشر اطلاعات | |
 |
این مقاله تحت شرایط Creative Commons Attribution-NonCommercial 4.0 International License قابل بازنشر است. |
