ArticleMedical science monitor : international medical journal of experimental and clinical research2019
Metformin Inhibit Lung Cancer Cell Growth and Invasion in Vitro as Well as Tumor Formation in Vivo Partially by Activating PP2A.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 40 citations in OpenAlex.
- Corynoxine Inhibits Tumor Growth via Targeting NQO1 and Modulating the PTPA-NQO1/PP2A Switch to Activate PP2A.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Hexaraphane as a potential therapeutic strategy for tauopathies.Redox biology · 2026Article
- Metformin Inhibits the Development of Lung Adenocarcinoma by Regulating the Expression of CCNA2Combinatorial chemistry & high throughput screening · 2026Article
- The therapeutic value of antidiabetic drugs in lung cancer treatment: from clinical evidence to possible mechanisms.Frontiers in immunology · 2026Review
- Metformin and its Nanoformulations in Cancer Prevention and Therapy.Current pharmaceutical design · 2025Review
- Anticarcinogenic Effects of Gold Nanoparticles and Metformin Against MCF-7 and A549 Cells.Biological trace element research · 2024Article
- Altering phosphorylation in cancer through PP2A modifiers.Cancer cell international · 2024Review
- [Research Progress on the Combination Therapy of EGFR-TKIs and Metformin in Acquired Resistance to EGFR-TKIs in Non-small Cell Lung Cancer].Zhongguo fei ai za zhi = Chinese journal of lung cancer · 2023Article
- Potential Mechanisms of Metformin-Induced Apoptosis in HeLa Cells.Biomolecules · 2023Article
- Research progress on the therapeutic effect and mechanism of metformin for lung cancer (Review).Oncology reports · 2023Review
- Metformin Mitigated Obesity-Driven Cancer Aggressiveness in Tumor-Bearing Mice.International journal of molecular sciences · 2022Article
- [Metformin and malignant neoplasms: a possible mechanism of antitumor action and prospects for use in practice].Problemy endokrinologii · 2022Article
- Advances in metformin‑based metabolic therapy for non‑small cell lung cancer (Review).Oncology reports · 2022Review
- Molecular mechanisms underlining the role of metformin as a therapeutic agent in lung cancer.Cellular oncology (Dordrecht, Netherlands) · 2021Review
- Metformin and Malignant Tumors: Not Over the Hill.Diabetes, metabolic syndrome and obesity : targets and therapy · 2021Review
- Metformin Increases Protein Phosphatase 2A Activity in Primary Human Skeletal Muscle Cells Derived from Lean Healthy Participants.Journal of diabetes research · 2021Article
- The effect of a novel glycolysis-related gene signature on progression, prognosis and immune microenvironment of renal cell carcinoma.BMC cancer · 2020Article
- Metformin induces caspase-dependent and caspase-independent apoptosis in human bladder cancer T24 cells.Anti-cancer drugs · 2020Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
BACKGROUND The aim of this study was to investigate whether PP2A activation is involved in the anti-cancer activity of metformin. MATERIAL AND METHODS A549 and H1651 human lung cancer cells were constructed with stable a4 overexpression (O/E α4) or knockdown of PP2A catalytic subunit A/B(sh-PP2Ac). Influences of okadaic acid (OA) treatment, O/E α4 or sh-PP2Ac on metformin treated cells were investigated by cell viability, proliferation, apoptosis, and Transwell invasion assay in vitro. Protein expression levels of Bax, Bcl-2, Myc, and Akt as well as serine phosphorylation level of Bax, Myc, and Akt were examined by western blot. For in vivo assays, wild type (WT) or modified A549 cells were subcutaneously injected in nude mice, and metformin treatment on these xenografted tumors were assayed by tumor formation assay and western blot detecting cell proliferation marker PCNA (proliferating cell nuclear antigen) as well as protein expression level and serine phosphorylation level of Akt and Myc. RESULTS Metformin treatment significantly reduced A549 or H1651 cell growth and invasive capacity in vitro as well as Ser184 phosphorylation of Bax, Ser62 phosphorylation of Myc, and Ser473 phosphorylation of Akt, all of which could be partially attenuated by OA treatment, O/E α4 or sh-PP2Ac. Metformin treatment also significantly reduced tumor formation in vivo as well as protein expression of PCNA, Akt, Myc, and serine phosphorylation of the latter 2, which can be partially blocked by O/E α4 or sh-PP2Ac. CONCLUSIONS Metformin reduced lung cancer cell growth and invasion in vitro as well as tumor formation in vivo partially by activating PP2A.
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