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DT-13 attenuates human lung cancer metastasis via regulating NMIIA activity under hypoxia condition
Xiao-Hui Wei1, Sen-Sen Lin2, Yang Liu1
1Jiangsu Center for Pharmacodynamics Research and Evaluation, China Pharmaceutical University, Nanjing, P.R. China.
Abstract:
Cancer metastasis plays a major role in tumor deterioration. Metastatic processes are known to be regulated by hypoxic microenvironment and non-muscle myosin IIA (NMIIA). DT-13, a bioactive saponin monomer isolated from Ophiopogon japonicus, has been reported to inhibit various cancer metastasis, but whether NMIIA is involved in the anti-metastatic activity of DT-13 under hypoxia remains to be determined. Thus, this study aims to clarify the role of DT-13 in regulating 95D cell metastasis under hypoxic microenvironment and to further investigate whether NMIIA is involved in the anti-metastatic mechanism of DT-13. We found that DT-13 significantly inhibited 95D cells metastasis in vitro and in vivo. Furthermore, hypoxia significantly inhibited the expression of NMIIA and redistributed NMIIA to the cell periphery, whereas DT-13 reversed the hypoxic effects by upregulating the expression of NMIIA. Moreover, DT-13 treatment redistributed NMIIA to the nuclear periphery and reduced the formation of F-actin in 95D cells. In addition, we found that the Raf-ERK1/2 signaling pathway is involved in regulation of NMIIA by DT-13. Collectively, these findings support NMIIA as a target of DT-13 to prevent lung cancer metastasis.
Insights
DT-13, a compound from Ophiopogon japonicus, inhibits lung cancer metastasis by targeting non-muscle myosin IIA (NMIIA). This study reveals DT-13 upregulates NMIIA expression, counteracting hypoxia
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Cancer metastasis is a critical factor in tumor progression.
- Hypoxic microenvironments and non-muscle myosin IIA (NMIIA) are key regulators of metastasis.
- DT-13, a saponin from Ophiopogon japonicus, shows anti-metastatic potential, but its mechanism involving NMIIA under hypoxia is unclear.
Purpose of the Study:
- To investigate the role of DT-13 in regulating 95D cell metastasis under hypoxia.
- To determine if NMIIA is involved in the anti-metastatic mechanism of DT-13.
Main Methods:
- In vitro and in vivo metastasis assays using 95D cells.
- Analysis of NMIIA expression and localization under hypoxic conditions with and without DT-13 treatment.
- Investigation of the Raf-ERK1/2 signaling pathway.
Main Results:
- DT-13 significantly inhibited 95D cell metastasis both in vitro and in vivo.
- Hypoxia decreased NMIIA expression and altered its cellular distribution, while DT-13 reversed these effects by upregulating NMIIA.
- DT-13 treatment led to NMIIA redistribution to the nuclear periphery and reduced F-actin formation, involving the Raf-ERK1/2 pathway.
Conclusions:
- DT-13 effectively inhibits lung cancer cell metastasis.
- NMIIA is a crucial target for DT-13's anti-metastatic activity, particularly under hypoxic conditions.
- The findings suggest DT-13 as a potential therapeutic agent for preventing lung cancer metastasis via NMIIA modulation.
