ArticleBioengineered2022
MACC1 regulates the AKT/STAT3 signaling pathway to induce migration, invasion, cancer stemness, and suppress apoptosis in cervical cancer cells.
Article in Bioengineered, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- Super-enhancer-driven EFNA1 fuels tumor progression in cervical cancer via the FOSL2-Src/AKT/STAT3 axis.The Journal of clinical investigation · 2025Article
- Prognostic risk stratification value of MACC1 expression in patients with gastric cancer.Clinical & translational oncology : official publication of the Federation of Spanish Oncology Societies and of the National Cancer Institute of Mexico · 2025Article
- MACC1 ablation suppresses the dedifferentiation process of non-CSCs in lung cancer through stabilizing KLF4.Cell death discovery · 2024Article
- MACC1 revisited - an in-depth review of a master of metastasis.Biomarker research · 2024Review
- Inhibition of STAT3 by 2-Methoxyestradiol suppresses M2 polarization and protumoral functions of macrophages in breast cancer.BMC cancer · 2024Article
- Biological functions and potential mechanisms of miR‑143‑3p in cancers (Review).Oncology reports · 2024Review
- Article
- Targeting Cervical Cancer Stem Cells by Phytochemicals.Current medicinal chemistry · 2024Review
- Review
- Tumor Necrosis Factor-Mediators of inflammation · 2023Article
- MACC1-Induced Collective Migration Is Promoted by Proliferation Rather Than Single Cell Biomechanics.Cancers · 2022Article
- Transcriptional factor 3 binds to sirtuin 1 to activate the Wnt/β-catenin signaling in cervical cancer.Bioengineered · 2022Article
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Cervical cancer (CC) ranks as the second most frequent tumor in women, and CC stem cells have been vital in the tumorigenesis of CC. Recently, the metastasis- associated in colon cancer 1 (MACC1) gene was proven to be a promising biomarker of CC. However, the role and mechanism of MACC1 in CC remain undetermined. Expressions of MACC1 were estimated by qRT-PCR, immunohistochemistry, and Western blot assays in cervical cancer tissues and cells. Three siRNAs were generated to knockdown expressions of MACC1 in CC cells. After knockdown of MACC1 or/and Colivelin treatment, cell migration, invasion, apoptosis, and stemness were evaluated through a series of functional experiments including Transwell, flow cytometry, Hoechst staining, and sphere-formation assays. MACC1 was found to express more highly in CC tissues in comparison with corresponding non-tumor tissues at both mRNA and protein levels. Functionally, the knocking- down of MACC1 significantly repressed migration and invasion, and induced apoptosis of CC cells. Also, knockdown of MACC1 was discovered to suppress sphere-formation of CC cells and downregulate OCT4 and Nanog. It was proved that knockdown of MACC1 had a significant blocking effect on the AKT/STAT3 pathway. In addition, we verified that treatment with the STAT3 activator (Colivelin) had significant reversal effects on the malignant behaviors of CC cells and CC stemness. Our study concluded that MACC1 might be a novel regulator of CC by regulating the AKT/STAT3 pathway to change the migration, invasion, apoptosis, and cancer stemness of CC cells.
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