Atractylenolide II reverses the influence of lncRNA XIST/miR‐30a‐5p/ROR1 axis on chemo‐resistance of colorectal cancer cells

Abstract

This investigation was conducted to elucidate whether atractylenolide II could reverse the role of lnc RNA XIST /miR‐30a‐5p/ ROR 1 axis in modulating chemosensitivity of colorectal cancer cells. We totally collected 294 pairs of colorectal cancer tissues and adjacent normal tissues and also purchased colorectal cancer cell lines and human embryonic kidney cell line. 5‐fluorouracil, cisplatin, mitomycin and adriamycin were designated as the chemotherapies for colorectal cell lines, and atractylenolides were arranged as the Chinese drug. The expressions of XIST , miR‐30a‐5p and ROR 1 were quantified with aid of qRT ‐ PCR or Western blot, and luciferase reporter gene assay was implemented to determine the relationships among XIST , miR‐30a‐5p and ROR 1. Our results demonstrated that XIST and ROR 1 expressions were dramatically up‐regulated, yet miR‐30a‐5p expression was down‐regulated within colorectal cancer tissues ( P < 0.05). The overexpressed XIST and ROR 1, as well as under‐expressed miR‐30a‐5p, were inclined to promote viability and proliferation of colorectal cells under the influence of chemo drugs ( P < 0.05). In addition, XIST could directly target miR‐30a‐5p, and ROR 1 acted as the targeted molecule of miR‐30a‐5p. Interestingly, atractylenolides not only switched the expressions of XIST , miR‐30a‐5p and ROR 1 within colorectal cancer cells but also significantly intensified the chemosensitivity of colorectal cancer cells ( P < 0.05). Finally, atractylenolide II was discovered to slow down the viability and proliferation of colorectal cancer cells ( P < 0.05). In conclusion, the XIST /miR‐30a‐5p/ ROR 1 axis could be deemed as pivotal markers underlying colorectal cancer, and administration of atractylenolide II might improve the chemotherapeutic efficacy for colorectal cancer.

Long noncoding RNA XIST enhances ethanol‐induced hepatic stellate cells autophagy and activation via miR‐29b/HMGB1 axis

“…For example, lncRNA H19 facilitates liver fibrosis by functioning as a ceRNA to sponge miR‐148a to sustain the expression of ubiquitin‐specific protease 4 (USP4) . Recent studies have suggested that XIST may serve as a ceRNA for miRNAs . In the present study, we investigated whether XIST can act as a ceRNA for miRNAs in HSCs activation and liver fibrosis.…”

A specific microRNA profile as predictive biomarker for systemic treatment in patients with metastatic colorectal cancer

“…[17][18][19][20] The other miRNAs, miR-30a-5p, miR-92b-3p, and miR-98-5p are involved in proliferation of CRC cells. [21][22][23] In addition, high expression of miR-92b-3p has previously been related to a prolonged progression-free survival in patients with mCRC treated with combined FOLFOX and bevacizumab. 24 The current study aimed to prospectively validate the predictive value of clinical benefit from systemic treatment of the previously identified miRNA signature in a cohort of patients with extensive mCRC, starting first-line palliative systemic therapy.…”

Transfer of metastatic traits via miR‐200c in extracellular vesicles derived from colorectal cancer stem cells is inhibited by atractylenolide I

“…More importantly, this ATL increased the chemosensitivity of CRC cells to conventional chemotherapeutic drugs including 5-fluorouracil, mitomycin, cisplatin, and Adriamycin, and this was achieved by modulating the lncRNA XIST/miR-30a-3p/ROR 1 axis. 42 Through our investigation, we found that the function of ATL-1 is twofold. On one hand, ATL-1 acted directly on CSCs by suppressing stemness maintenance and promoting CSC apoptosis.…”