Related Experiment Video
Updated: Jul 30, 2025

Studying Pancreatic Cancer Stem Cell Characteristics for Developing New Treatment Strategies
Published on: June 20, 2015
Metformin sensitises osteosarcoma to chemotherapy via the IGF-1R/miR-610/FEN1 pathway
Suwei Dong1, Yanbin Xiao2, Ziqiang Zhu3
1Department of Orthopaedics, The Second Affiliated Hospital of Xuzhou Medical University, Xuzhou, Jiangsu; Department of Orthopaedics, The Third Affiliated Hospital of Kunming Medical University, Kunming, Yunnan. dong.suwei@163.com.
Abstract:
Metformin can enhance cancer cell chemosensitivity to anticancer drugs. IGF-1R is involved in cancer chemoresistance. The current study aimed to elucidate the role of metformin in osteosarcoma (OS) cell chemosensitivity modulation and identify its underlying mechanism in IGF-1R/miR-610/FEN1 signalling. IGF-1R, miR-610, and FEN1 were aberrantly expressed in OS and participated in apoptosis modulation; this effect was abated by metformin treatment. Luciferase reporter assays confirmed that FEN1 is a direct target of miR-610. Moreover, metformin treatment decreased IGF-1R and FEN1 but elevated miR-610 expression. Metformin sensitised OS cells to cytotoxic agents, while FEN1 overexpression partly compromised metformin's sensitising effects. Furthermore, metformin was observed to enhance adriamycin's effects in a murine xenograft model. Metformin enhanced OS cell sensitivity to cytotoxic agents via the IGF-1R/miR-610/FEN1 signalling axis, highlighting its potential as an adjuvant during chemotherapy.
Related Concept Videos
Oral Hypoglycemic Agents: Biguanides and Glitazones
mTOR Signaling and Cancer Progression
The mTOR pathway or the...
Mitogens and the Cell Cycle
Targeted Cancer Therapies
There are several types of targeted therapies against...

