Add like
Add dislike
Add to saved papers

Long non-coding RNA DINO promotes cisplatin sensitivity in lung adenocarcinoma via the p53-Bax axis.

BACKGROUND: The damage-induced non-coding ( DINO ) RNA is a newly identified long non-coding RNA (lncRNA) found in human cells with DNA damage. The treatment of tumors with cisplatin can induce DNA damage; however, whether the lncRNA DINO is involved in the treatment of non-small cell lung cancer (NSCLC) has not yet been elucidated.

METHODS: The expression of the lncRNA DINO in lung adenocarcinoma cells was detected using quantitative real-time polymerase chain reaction (qRT-PCR). The lung adenocarcinoma cell line, A549, and derived cisplatin-resistant cell line, A549R, were selected to construct cell models with lncRNA DINO overexpression or interference via lentiviral transfection. After cisplatin treatment, changes in the apoptosis rate were measured. Changes in the p53-Bax axis were detected by qRT-PCR and Western blot. Cycloheximide (CHX) interference demonstrated the stability of p53 with new protein production induced by the lncRNA DINO . The in vivo experiments involved intraperitoneal injection of nude mice with cisplatin after subcutaneous tumor formation, and the tumor diameters and weights were recorded. Immunohistochemistry and hematoxylin and eosin (H&E) staining were performed following tumor removal.

RESULTS: We found that the lncRNA DINO was significantly down-regulated in NSCLC. DINO overexpression enhanced the sensitivity of NSCLC cells to cisplatin, while DINO down-regulation decreased the sensitivity of NSCLC cells to cisplatin. Mechanistic investigation indicated that DINO enhanced the stability of p53 and mediated the activation of the p53-Bax signaling axis. Our results also demonstrated that the lncRNA DINO could partially reverse cisplatin resistance induced by silencing the p53-Bax axis, and could inhibit subcutaneous tumorigenesis in nude mice after cisplatin treatment in vivo .

CONCLUSIONS: The lncRNA DINO regulates the sensitivity of lung adenocarcinoma to cisplatin by stabilizing p53 and activating the p53-Bax axis, and thus, may be a novel therapeutic target to overcome cisplatin resistance.

Full text links

We have located links that may give you full text access.
Can't access the paper?
Try logging in through your university/institutional subscription. For a smoother one-click institutional access experience, please use our mobile app.

Related Resources

For the best experience, use the Read mobile app

Mobile app image

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app

All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.

By using this service, you agree to our terms of use and privacy policy.

Your Privacy Choices Toggle icon

You can now claim free CME credits for this literature searchClaim now

Get seemless 1-tap access through your institution/university

For the best experience, use the Read mobile app