ArticleBioengineered2021
Meis homeobox 2 (MEIS2) inhibits the proliferation and promotes apoptosis of thyroid cancer cell and through the NF-κB signaling pathway.
Article in Bioengineered, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 14 citations in OpenAlex.
- Pathogenic role and therapeutic targets of nuclear factor-κB signaling pathway in cancer (Review).Oncology letters · 2025Review
- Development and validation of a necroptosis-related gene signature for predicting prognosis and immune infiltration in papillary thyroid cancer.Translational cancer research · 2025Article
- HOX and MEINOX in cellular plasticity, fibrosis, and cancer.World journal of stem cells · 2025Review
- Targeting GSK3β and signaling pathways in breast cancer: role of individual members of miR- 23/24/27 cluster.BMC cancer · 2025Article
- A Newly Characterized, Two BRCT Domain-Containing Isoform of PAX-Interacting Protein (PTIP) Generated via Frame Shift and Alternative Pre-mRNA Splicing.Journal of cellular signaling · 2025Article
- Myeloid ectopic viral integration site 2 accelerates the progression of Alzheimer's disease.Aging cell · 2024Article
- Cleft palate, congenital heart disease, and developmental delay involvingFrontiers in pediatrics · 2024Article
- Role of ADAM33 short isoform as a tumor suppressor in the pathogenesis of thyroid cancer via oncogenic function disruption of full-length ADAM33.Human cell · 2023Article
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
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Abstract
Investigation of effects of Meis homeobox 2 (MEIS2) on proliferation and apoptosis of thyroid cancer (TC) cells and its specific molecular mechanism is the main purpose of this study. In this study, we found that the expression of MEIS2 was down-regulated in TC tissues and cell lines (B-CPAP, TPC-1 and K1), compared to adjacent histologically normal tissues and normal thyroid cell (Nthy-ori 3-1). Then, overexpression of MEIS2 promoted B-CPAP cell apoptosis and decreased cell proliferation, viability and cell cycle progression. Further studies confirmed that overexpression of MEIS2 could significantly decrease p65 expression in the nucleus of B-CPAP cells. However, the opposite results were presented after interference of MEIS2 expression. Taken together, MEIS2 expression was significantly down-regulated in TC. In addition, MEIS2 could inhibit NF-κB pathway activation, so as to perform both suppression of the viability and proliferation of TC cells and promotion of apoptosis.
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