Skip to content
DraconiticResearch
Search Sources API
203,234 studies31 sourcesUpdated 32 min ago
Peer-reviewedCC BY-NC-ND 4.0Cancer Medicine

Oncogenic hsa_circ_0000247 Promotes Breast Cancer Malignancy Through hsa‐let‐7i‐5p Sponging‐Mediated HMGA1 Upregulation

4 affiliations
  1. 1Department of Laboratory Medicine The Second Affiliated Hospital of Wannan Medical College Wuhu Anhui P.R. China
  2. 2Department of Urology The Second Affiliated Hospital of Wannan Medical College Wuhu Anhui P.R. China
  3. 3Interventional Department The First Affiliated Hospital of Wannan Medical College Wuhu Anhui P.R. China
  4. 4Department of Thyroid and Breast Surgery The Second Affiliated Hospital of Wannan Medical College Wuhu Anhui P.R. China

Abstract

Circular RNAs (circRNAs) are stable, evolutionarily conserved non‐coding RNAs with covalently closed‐loop structures, which function as oncogenes or tumor suppressors to regulate cancer cell proliferation, invasion, metastasis, and apoptosis. This study explored the role and regulatory mechanism of hsa_circ_0000247 in breast cancer. The expression levels of hsa_circ_0000247, hsa‐let‐7i‐5p, and HMGA1 were detected by RT‐qPCR and western blotting. Biological functions were evaluated using CCK‐8, EdU, colony formation, Transwell, flow cytometry, and electron microscopy assays. The interactions among hsa_circ_0000247, hsa‐let‐7i‐5p, and HMGA1 were verified by dual‐luciferase reporter assays, and rescue experiments were conducted. Hsa_circ_0000247 was significantly upregulated in 30 pairs of breast cancer tissues and MCF‐7, MDA‐MB‐231, and BT‐474 cell lines. Knockdown of hsa_circ_0000247 inhibited cell proliferation, migration, and invasion, and promoted apoptosis. Mechanistically, hsa_circ_0000247 directly sponged hsa‐let‐7i‐5p, which targeted the 3′UTR of HMGA1. Inhibition of hsa‐let‐7i‐5p reversed the effects of hsa_circ_0000247 silencing. In conclusion, hsa_circ_0000247 is upregulated in breast cancer and promotes malignant progression via the hsa_circ_0000247/hsa‐let‐7i‐5p/HMGA1 axis, providing a potential diagnostic and therapeutic target for breast cancer.

Related

  1. Oncogenic CLDN1 promotes thyroid cancer progression through TAp63-mediated glycolytic switching
    Bowei Zhang, Jinju Wang, Qianxi Zhang +1
    iSciencePeer-reviewedCC BY 4.0Molecular biology & gene regulationCell biologyCrossrefCell Press
  2. FAM50A promotes esophageal squamous cell carcinoma progression via splicing-dependent oncogenic circSDK1- and DUSP22-mediated MAPK/FAK activation.
    Yan Bian, Ye Gao, Xin Chang +7
    Cell discoveryPeer-reviewedCC BYFull textMolecular biology & gene regulationEurope PMCDOAJ
  3. hsa_circ_0001377 promotes hepatic fibrosis by sponging let-7a-5p and targeting TGFBR1, Smad2, and Col1a2
    Jiaming Zhou, Jiaxuan Liu, Dikun Wu +3
    Frontiers in pharmacologyPeer-reviewedCC BYFull textMolecular biology & gene regulationEurope PMCCrossref
  4. Acidic bile salt-induced DNA methylation promotes APE1 upregulation through miR-128-3p silencing in esophageal adenocarcinoma
    FARAH BALLOUT, HENG LU, LEI CHEN +9
    Oncology reportsPeer-reviewedCC BY-NC-NDFull textMolecular biology & gene regulationEurope PMCPMC
  5. BCAM-AKT2 fusion protein promotes unfolded protein response driven oncogenic signaling in SKOV3 epithelial ovarian cancer cell line
    Hala Khazem, Ravid Solomon Zemler, Liron Vardi David +5
    PLOS OnePeer-reviewedCC BY 4.0Full textMolecular biology & gene regulationStatisticsPLOS
BibTeX
@article{qin2026oncogenic,
  title = {{Oncogenic hsa_circ_0000247 Promotes Breast Cancer Malignancy Through hsa‐let‐7i‐5p Sponging‐Mediated HMGA1 Upregulation}},
  author = {Mingming Qin and Xue Chai and Kai Ye and Ping Zhu and Tong Lu and Zhifeng Hu and Zhiyong Zhao and Jun Bao and Jing Wu},
  journal = {Cancer Medicine},
  year = {2026},
  month = nov,
  doi = {10.1002/cam4.72249},
  url = {https://doi.org/10.1002/cam4.72249},
  note = {CC BY-NC-ND 4.0},
}
RIS
TY  - JOUR
TI  - Oncogenic hsa_circ_0000247 Promotes Breast Cancer Malignancy Through hsa‐let‐7i‐5p Sponging‐Mediated HMGA1 Upregulation
AU  - Mingming Qin
AU  - Xue Chai
AU  - Kai Ye
AU  - Ping Zhu
AU  - Tong Lu
AU  - Zhifeng Hu
AU  - Zhiyong Zhao
AU  - Jun Bao
AU  - Jing Wu
PY  - 2026
DA  - 2026/11/05
JO  - Cancer Medicine
DO  - 10.1002/cam4.72249
UR  - https://doi.org/10.1002/cam4.72249
AB  - Circular RNAs (circRNAs) are stable, evolutionarily conserved non‐coding RNAs with covalently closed‐loop structures, which function as oncogenes or tumor suppressors to regulate cancer cell proliferation, invasion, metastasis, and apoptosis. This study explored the role and regulatory mechanism of hsa_circ_0000247 in breast cancer. The expression levels of hsa_circ_0000247, hsa‐let‐7i‐5p, and HMGA1 were detected by RT‐qPCR and western blotting. Biological functions were evaluated using CCK‐8, EdU, colony formation, Transwell, flow cytometry, and electron microscopy assays. The interactions among hsa_circ_0000247, hsa‐let‐7i‐5p, and HMGA1 were verified by dual‐luciferase reporter assays, and rescue experiments were conducted. Hsa_circ_0000247 was significantly upregulated in 30 pairs of breast cancer tissues and MCF‐7, MDA‐MB‐231, and BT‐474 cell lines. Knockdown of hsa_circ_0000247 inhibited cell proliferation, migration, and invasion, and promoted apoptosis. Mechanistically, hsa_circ_0000247 directly sponged hsa‐let‐7i‐5p, which targeted the 3′UTR of HMGA1. Inhibition of hsa‐let‐7i‐5p reversed the effects of hsa_circ_0000247 silencing. In conclusion, hsa_circ_0000247 is upregulated in breast cancer and promotes malignant progression via the hsa_circ_0000247/hsa‐let‐7i‐5p/HMGA1 axis, providing a potential diagnostic and therapeutic target for breast cancer.
SN  - 2045-7634
ER  -