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Updated: May 30, 2025

Quantitative PCR-based Assay to Measure Sonic Hedgehog Signaling in Cellular Model of Ciliogenesis
Published on: January 31, 2025
Hsa_circ_0000105 promotes nasopharyngeal carcinoma malignancy by miR-541-3p/S100A11 axis
LuXing Peng1, Jian Qin1, DeFeng Qing2
1Department of Clinical Oncology Center, Radiotherapy Ward 3, The People's Hospital of Guangxi Zhuang Autonomous Region, Nanning City, Guangxi Zhuang Autonomous Region, China.
Objective:
This study was to investigate whether hsa_circ_0000105 is involved in the process of regulating Nasopharyngeal Carcinoma (NPC) biological behaviors and to reveal the molecular mechanism.
Methods:
NPC tissues and normal tissues were collected, and NPC cell lines and normal control cell lines were obtained. hsa_circ_0000105/miR-541-3p/S100A11 was evaluated by RT-qPCR or Western blot. CCK-8 assay, EdU assay, Transwell assay, wound healing assay, flow cytometry, and Western blot were employed to evaluate the biological behaviors of NPC cells. Dual luciferase reporter assay and RIP assay were applied to evaluate the direct targeting relationship of hsa_circ_0000105/miR-541-3p/S100A11. A tumor xenotransplantation assay was implemented to evaluate the effect of hsa_circ_0000105 on NPC tumors.
Results:
hsa_circ_0000105 and S100A11 were highly expressed in NPC, while miR-541-3p was lowly expressed. hsa_circ_0000105 competitively adsorbed miR-541-3p and mediated S100A11 expression. Silencing or upregulation of hsa_circ_0000105 restricts and induces malignant behavior in HNE2 cells, respectively. The impact of hsa_circ_0000105 silencing on malignant behaviors of HNE2 cells was blocked by miR-541-3p downregulation, while that of hsa_circ_0000105 upregulation was attenuated by S100A11 inhibition.
Conclusion:
hsa_circ_0000105 acts as a carcinogenic factor in NPC and promotes NPC malignancy by miR-541-3p/S100A11 axis.
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