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Multi-omics sequencing revealed endostar combined with cisplatin treated non small cell lung cancer via
Yufei Wang1,2, Hong Ren3
1Department of Thoracic Surgery, The First Affiliated Hospital of Xi'an Jiaotong University, No. 277 West Yanta Road, 710061, Shanxi, Xi'an, Shanxi, P.R. China.
Background:
Endostar, an anti-angiogenic drug, has been approved for treating non-small cell lung cancer (NSCLC). At present, endostar combined with radiotherapy or chemotherapy has achieved ideal results in the treatment of some tumors, but there is a lack of application and study in NSCLC. This study investigated the therapeutic effect and potential mechanism of endostar combined with cisplatin (EC) in NSCLC.
Methods:
HE staining, TUNEL staining, immunofluorescence, colony formation ability, and cell migration ability were used to evaluate the anti-tumor activity of EC. The expressions of FMOD, VEGF, FGF-2, and PDGF-B were detected by western blotting and qPCR. The target of combination therapy was analyzed by m6A sequencing and RNA sequencing. METTL3 knockdown and overexpressed A549 cells were constructed and co-cultured with HUVECs to further evaluate the effect of METLL3 on combination therapy.
Results:
Combination therapy significantly reduced the colony formation and migration ability of NSCLC cells, induced cell apoptosis, and inhibited the tube formation ability of HUVECs. The results of m6A sequencing and RNA sequencing showed that the EC could down-regulate the expression level of FMOD in tumor tissues, which might be related to the reduction of its m6A methylation modification regulatory enzyme METTL3. Restricting FMOD expression could reduce the expression of FGF2, TGF-β1, VEGF and PDGF-B. Moreover, overexpression of METTLE almost abolished the anti-tumor effect of EC and promoted angiogenesis.
Conclusions:
Endostar combined with cisplatin might exert anti-tumor effects by down-regulating the expression of METTL3 and FMOD.
Insights
Endostar and cisplatin combination therapy shows promise for non-small cell lung cancer (NSCLC) treatment. This approach may work by reducing METTL3 and FMOD expression, inhibiting tumor growth and angiogenesis.
Area of Science:
- Oncology
- Molecular Biology
- Cancer Research
Background:
- Endostar, an anti-angiogenic drug, is approved for non-small cell lung cancer (NSCLC).
- Combination therapy with Endostar shows potential but lacks study in NSCLC.
- This study investigates Endostar combined with cisplatin (EC) in NSCLC.
Purpose of the Study:
- To evaluate the therapeutic effect of EC in NSCLC.
- To elucidate the potential mechanism of EC action.
- To investigate the role of METTL3 and FMOD in EC's anti-tumor activity.
Main Methods:
- Assessed anti-tumor activity using HE staining, TUNEL, immunofluorescence, colony formation, and migration assays.
- Quantified expressions of FMOD, VEGF, FGF-2, and PDGF-B via western blotting and qPCR.
- Utilized m6A and RNA sequencing to identify therapeutic targets and constructed METTL3 knockdown/overexpression cells for mechanistic studies.
Main Results:
- EC significantly inhibited NSCLC cell proliferation, migration, and induced apoptosis, while suppressing HUVEC tube formation.
- EC down-regulated FMOD expression, potentially via reduced METTL3 m6A methylation.
- FMOD downregulation decreased expression of angiogenesis factors (FGF2, TGF-β1, VEGF, PDGF-B); METTL3 overexpression abolished EC's anti-tumor effects.
Conclusions:
- Endostar and cisplatin combination therapy demonstrates significant anti-tumor effects in NSCLC.
- The mechanism involves down-regulating METTL3 and FMOD expression.
- This combination therapy offers a potential strategy for NSCLC treatment.
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