Published online Jan 28, 2024. doi: 10.3748/wjg.v30.i4.367
Peer-review started: December 12, 2023
First decision: December 19, 2023
Revised: December 21, 2023
Accepted: January 3, 2024
Article in press: January 3, 2024
Published online: January 28, 2024
Processing time: 45 Days and 4.1 Hours
Esophageal cancer (EC) is the sixth most common tumor worldwide and has a poor prognosis. Although L-type calcium channel blockers have demonstrated efficacy in inhibiting the occurrence and development of various tumors, their impact on EC remains unclear.
Patients with EC have a poor prognosis owing to a lack of effective treatments and prognostic indicators. This study aimed to explore a novel approach for treating EC and improving patient survival rates.
To elucidate the mechanism by which the L-type calcium channel blocker, amlodipine, inhibits the proliferation and migration of EC cells, thereby offering a potential new avenue for the treatment of EC.
Western blot analysis was used to assess the expression of relevant proteins. Cell migration was evaluated using Transwell assays and apoptosis was measured using flow cytometry. The endoplasmic reticulum (ER) stress inhibitor 4-phenylbutyric acid was used to prevent ER stress. Transduction of EC cells with GFP-RFP-LC3 adenovirus confirmed that amlodipine-mediated ER stress functions through downstream autophagy. In addition, a murine xenograft model constructed using Eca109 cells was used to validate the anti-tumor effects of amlodipine in vivo.
This study revealed that the Cav1.3 level in EC tissues was higher than that in adjacent tissues. The L-type calcium channel blocker, amlodipine, inhibits the proliferation and migration of EC cells while promoting apoptosis. Mechanistic investigations have indicated that these effects are associated with the induction of cellular ER stress. Further studies using GFP-RFP-LC3 adenovirus-transfected cells treated with amlodipine demonstrated that autophagy, mediated by ER stress, played a protective role in this process. In addition, amlodipine inhibited EC cell growth and presented an antitumor effect in vivo.
L-type calcium channels are highly expressed in EC tissues. Both in vivo and in vitro experiments revealed that amlodipine inhibited the proliferation and migration of EC cells through ER stress.
The expression levels of L-type calcium channels in EC may serve as an index of prognosis, and the combination of amlodipine with autophagy inhibitors holds promise as a novel treatment approach. Future endeavors should involve large-sample multicenter clinical studies to further validate its reliability.