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Updated: Mar 2, 2026

Induction of Mesenchymal-Epithelial Transitions in Sarcoma Cells
Published on: April 7, 2017
Knockdown of STMN1 enhances osteosarcoma cell chemosensitivity through inhibition of autophagy
Zili Wang1, Rongzhen He1, Hansong Xia1
1Department of Orthopaedic Surgery, The Third Xiangya Hospital of Central South University, Changsha, Hunan 410013, P.R. China.
Abstract:
Chemoresistance is a major cause for the poor prognosis of osteosarcoma (OS) patients. However, our understanding of mechanisms underlying chemoresistance in OS are limited. The present study aimed to investigate the effect of stathmin 1 (STMN1) on paclitaxel-induced chemoresistance, as well as the underlying mechanism. Western blot analysis data revealed that the expression level of STMN1 was dramatically increased in OS cell lines (HOS, Saos-2, U-2OS and MG-63), when compared to normal osteoblast hFOB1.19 cells. Furthermore, treatment with paclitaxel led to upregulation of STMN1 in U-2OS cells, accompanied by activation of autophagy, which may attenuate the cytotoxicity of paclitaxel in OS cells. Following knockdown of STMN1 expression, paclitaxel-induced autophagy was significantly reduced, accompanied by increased cytotoxicity of paclitaxel to U-2OS cells. In addition, blockade of mammalian target of rapamycin signaling attenuated the inhibitory effect of STMN1 knockdown on autophagy in OS cells. In conclusion, the present study demonstrated that knockdown of STMN1 enhances osteosarcoma cell chemosensitivity to paclitaxel through inhibition of autophagy. Therefore, STMN1 may be a potential target for the treatment of chemoresistant OS.
Insights
Stathmin 1 (STMN1) promotes chemoresistance in osteosarcoma by activating autophagy. Reducing STMN1 enhances sensitivity to paclitaxel by inhibiting this process, offering a potential therapeutic target.
Area of Science:
- Oncology
- Molecular Biology
- Cell Biology
Background:
- Chemoresistance significantly impacts osteosarcoma (OS) patient outcomes.
- Mechanisms driving OS chemoresistance remain incompletely understood.
Purpose of the Study:
- To investigate the role of stathmin 1 (STMN1) in paclitaxel-induced chemoresistance in OS.
- To elucidate the underlying molecular mechanisms involving autophagy.
Main Methods:
- Western blot analysis to assess STMN1 expression in OS cell lines and normal osteoblasts.
- Paclitaxel treatment to induce chemoresistance and autophagy.
- STMN1 knockdown experiments.
- Mammalian target of rapamycin (mTOR) signaling pathway blockade.
Main Results:
- STMN1 expression was significantly elevated in multiple OS cell lines compared to normal cells.
- Paclitaxel treatment upregulated STMN1 and activated autophagy in U-2OS cells.
- Knockdown of STMN1 reduced paclitaxel-induced autophagy and increased cancer cell sensitivity to paclitaxel.
- mTOR pathway inhibition partially reversed the effect of STMN1 knockdown on autophagy.
Conclusions:
- STMN1 promotes chemoresistance in osteosarcoma by enhancing paclitaxel-induced autophagy.
- Targeting STMN1 can improve osteosarcoma chemosensitivity to paclitaxel via autophagy inhibition.
- STMN1 represents a promising therapeutic target for overcoming chemoresistance in OS.
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