Abstract
Colorectal cancer (CRC) is a fatal disease ranking the third among the commonplace cancer types around the world. It is extremely significant to exploit effective treatments against CRC. FAM225A was proved to influence cell progression and forecast unfavorable prognosis in nasopharyngeal carcinoma. The role and function mechanism of FAM225A are still unclear in CRC. In this research, FAM225A was discovered presenting much higher expression in CRC tissues and cell lines. In addition, depleting FAM225A was capable of inhibiting cell proliferation, migration, and epithelial‐to‐mesenchymal transition (EMT) progress, and enhancing cell apoptosis ability. Furthermore, miR‐613 exerted important effects as a mediator between FAM225A and NOTCH3. NOTCH3 was negatively correlated with miR‐613, whereas was positively associated with FAM225A. Via competitively binding with miR‐613, FAM225A positively regulated NOTCH3 expression. FAM225A facilitated CRC occurrence and development through positively regulating NOTCH3 expression by binding with miR‐613. In a word, FAM225A/miR‐613/NOTCH3 axis may play a tumor‐facilitator in CRC cell progression. These data manifested the pivotal effect of FAM225A/miR‐613/NOTCH3 pathway in CRC cell proliferation, apoptosis, and migration process. The findings may provide some theoretical basis and different perspective for CRC treatment.
Highlights
Colorectal cancer (CRC) is a fatal disease ranking third among the commonplace cancer types around the world.[1]
We found that FAM225A showed much lower expression in normal colon epithelial cell line FHC than in CRC cell lines (Figure 1D)
As the downstream gene of FAM225A, miR-613 could bind to FAM225A and inversely associated with it
Summary
Colorectal cancer (CRC) is a fatal disease ranking third among the commonplace cancer types around the world.[1]. Long noncoding RNAs (lncRNAs) have become new hot spots for disease treatment, especially for cancers.[8,9] Recently, multiple researches revealed that lncRNAs exerted important effects during genesis, development, and progression of human tumors, as well as served as the driving factors of carcinogenic function via many mechanisms.[10,11,12,13] some lncRNAs were associated with cell fate and gene expression in the development and progression of several cancers, including CRC. Working as a competing endogenous RNA (ceRNA), FAM225A could upregulate ITGB3 via binding with miR-590-3p in NPC.[17] the role and function mechanism of FAM225A are still unclear in CRC. This paper may offer new perspectives for searching biomarkers for CRC treatment
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