Dihydroartemisinin targets the miR-497-5p/SOX5 axis to suppress tumor progression in non-small cell lung cancer
IntroductionNon-small cell lung cancer (NSCLC) remains a lethal malignancy with limited therapeutic options. Although dihydroartemisinin (DHA) exhibits anticancer properties, its mechanisms in NSCLC are incompletely understood. This study investigated the role of the miR-497-5p/SOX5 axis in mediatin...
Saved in:
| Main Authors: | , , , , , , , , , , , , |
|---|---|
| Format: | Article |
| Language: | English |
| Published: |
Frontiers Media S.A.
2025-07-01
|
| Series: | Frontiers in Pharmacology |
| Subjects: | |
| Online Access: | https://www.frontiersin.org/articles/10.3389/fphar.2025.1605531/full |
| Tags: |
Add Tag
No Tags, Be the first to tag this record!
|
| _version_ | 1849415617322418176 |
|---|---|
| author | Qing-Hua Yin Qiang Zhou Jian-Bing Hu Jie Weng Er-Dong Shen Fang Wen Song-Lian Liu Lei-Lan Yin Ya-Jun Tong Ling Long Ke-Wei Tang Si-Te Bai Lu-Di Ou |
| author_facet | Qing-Hua Yin Qiang Zhou Jian-Bing Hu Jie Weng Er-Dong Shen Fang Wen Song-Lian Liu Lei-Lan Yin Ya-Jun Tong Ling Long Ke-Wei Tang Si-Te Bai Lu-Di Ou |
| author_sort | Qing-Hua Yin |
| collection | DOAJ |
| description | IntroductionNon-small cell lung cancer (NSCLC) remains a lethal malignancy with limited therapeutic options. Although dihydroartemisinin (DHA) exhibits anticancer properties, its mechanisms in NSCLC are incompletely understood. This study investigated the role of the miR-497-5p/SOX5 axis in mediating DHA’s effects on NSCLC.MethodsIn vitro experiments utilized A549 and H1299 cells treated with DHA (50 μM). Proliferation, migration, invasion, and apoptosis were assessed. miR-497-5p and SOX5 expression was modulated via genetic silencing. In vivo, A549 xenograft tumor growth in mice was evaluated under DHA treatment (25/50 mg/kg).ResultsDHA significantly suppressed proliferation, migration, and invasion while inducing apoptosis in vitro. Mechanistically, DHA upregulated miR-497-5p and downregulated SOX5—overexpressed in clinical NSCLC. Silencing miR-497-5p attenuated DHA’s effects and increased SOX5, whereas SOX5 knockdown reversed miR-497-5p inhibition. In vivo, DHA dose-dependently inhibited tumor growth with miR-497-5p elevation and SOX5 suppression, effects abrogated by miR-497-5p inhibition but rescued by SOX5 knockdown.DiscussionDHA exerts antitumor activity by activating the miR-497-5p/SOX5 axis, revealing a novel mechanism. Bridging efficacious in vitro concentrations with clinically achievable dosing remains essential for therapeutic translation. |
| format | Article |
| id | doaj-art-5b2e3fdcb8234a55a0612c5ea3eb9315 |
| institution | Kabale University |
| issn | 1663-9812 |
| language | English |
| publishDate | 2025-07-01 |
| publisher | Frontiers Media S.A. |
| record_format | Article |
| series | Frontiers in Pharmacology |
| spelling | doaj-art-5b2e3fdcb8234a55a0612c5ea3eb93152025-08-20T03:33:27ZengFrontiers Media S.A.Frontiers in Pharmacology1663-98122025-07-011610.3389/fphar.2025.16055311605531Dihydroartemisinin targets the miR-497-5p/SOX5 axis to suppress tumor progression in non-small cell lung cancerQing-Hua YinQiang ZhouJian-Bing HuJie WengEr-Dong ShenFang WenSong-Lian LiuLei-Lan YinYa-Jun TongLing LongKe-Wei TangSi-Te BaiLu-Di OuIntroductionNon-small cell lung cancer (NSCLC) remains a lethal malignancy with limited therapeutic options. Although dihydroartemisinin (DHA) exhibits anticancer properties, its mechanisms in NSCLC are incompletely understood. This study investigated the role of the miR-497-5p/SOX5 axis in mediating DHA’s effects on NSCLC.MethodsIn vitro experiments utilized A549 and H1299 cells treated with DHA (50 μM). Proliferation, migration, invasion, and apoptosis were assessed. miR-497-5p and SOX5 expression was modulated via genetic silencing. In vivo, A549 xenograft tumor growth in mice was evaluated under DHA treatment (25/50 mg/kg).ResultsDHA significantly suppressed proliferation, migration, and invasion while inducing apoptosis in vitro. Mechanistically, DHA upregulated miR-497-5p and downregulated SOX5—overexpressed in clinical NSCLC. Silencing miR-497-5p attenuated DHA’s effects and increased SOX5, whereas SOX5 knockdown reversed miR-497-5p inhibition. In vivo, DHA dose-dependently inhibited tumor growth with miR-497-5p elevation and SOX5 suppression, effects abrogated by miR-497-5p inhibition but rescued by SOX5 knockdown.DiscussionDHA exerts antitumor activity by activating the miR-497-5p/SOX5 axis, revealing a novel mechanism. Bridging efficacious in vitro concentrations with clinically achievable dosing remains essential for therapeutic translation.https://www.frontiersin.org/articles/10.3389/fphar.2025.1605531/fulldihydroartemisinin (DHA)non-small cell lung cancer (NSCLC)miR-497-5pSOX5anticancer activity |
| spellingShingle | Qing-Hua Yin Qiang Zhou Jian-Bing Hu Jie Weng Er-Dong Shen Fang Wen Song-Lian Liu Lei-Lan Yin Ya-Jun Tong Ling Long Ke-Wei Tang Si-Te Bai Lu-Di Ou Dihydroartemisinin targets the miR-497-5p/SOX5 axis to suppress tumor progression in non-small cell lung cancer Frontiers in Pharmacology dihydroartemisinin (DHA) non-small cell lung cancer (NSCLC) miR-497-5p SOX5 anticancer activity |
| title | Dihydroartemisinin targets the miR-497-5p/SOX5 axis to suppress tumor progression in non-small cell lung cancer |
| title_full | Dihydroartemisinin targets the miR-497-5p/SOX5 axis to suppress tumor progression in non-small cell lung cancer |
| title_fullStr | Dihydroartemisinin targets the miR-497-5p/SOX5 axis to suppress tumor progression in non-small cell lung cancer |
| title_full_unstemmed | Dihydroartemisinin targets the miR-497-5p/SOX5 axis to suppress tumor progression in non-small cell lung cancer |
| title_short | Dihydroartemisinin targets the miR-497-5p/SOX5 axis to suppress tumor progression in non-small cell lung cancer |
| title_sort | dihydroartemisinin targets the mir 497 5p sox5 axis to suppress tumor progression in non small cell lung cancer |
| topic | dihydroartemisinin (DHA) non-small cell lung cancer (NSCLC) miR-497-5p SOX5 anticancer activity |
| url | https://www.frontiersin.org/articles/10.3389/fphar.2025.1605531/full |
| work_keys_str_mv | AT qinghuayin dihydroartemisinintargetsthemir4975psox5axistosuppresstumorprogressioninnonsmallcelllungcancer AT qiangzhou dihydroartemisinintargetsthemir4975psox5axistosuppresstumorprogressioninnonsmallcelllungcancer AT jianbinghu dihydroartemisinintargetsthemir4975psox5axistosuppresstumorprogressioninnonsmallcelllungcancer AT jieweng dihydroartemisinintargetsthemir4975psox5axistosuppresstumorprogressioninnonsmallcelllungcancer AT erdongshen dihydroartemisinintargetsthemir4975psox5axistosuppresstumorprogressioninnonsmallcelllungcancer AT fangwen dihydroartemisinintargetsthemir4975psox5axistosuppresstumorprogressioninnonsmallcelllungcancer AT songlianliu dihydroartemisinintargetsthemir4975psox5axistosuppresstumorprogressioninnonsmallcelllungcancer AT leilanyin dihydroartemisinintargetsthemir4975psox5axistosuppresstumorprogressioninnonsmallcelllungcancer AT yajuntong dihydroartemisinintargetsthemir4975psox5axistosuppresstumorprogressioninnonsmallcelllungcancer AT linglong dihydroartemisinintargetsthemir4975psox5axistosuppresstumorprogressioninnonsmallcelllungcancer AT keweitang dihydroartemisinintargetsthemir4975psox5axistosuppresstumorprogressioninnonsmallcelllungcancer AT sitebai dihydroartemisinintargetsthemir4975psox5axistosuppresstumorprogressioninnonsmallcelllungcancer AT ludiou dihydroartemisinintargetsthemir4975psox5axistosuppresstumorprogressioninnonsmallcelllungcancer |