ArticleInternational journal of molecular sciences2022
Interaction of MRPL9 and GGCT Promotes Cell Proliferation and Migration by Activating the MAPK/ERK Pathway in Papillary Thyroid Cancer.
Article in International journal of molecular sciences, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
16 citing papers in PubMed, 22 citations in OpenAlex.
- Metabolic orchestration driven by GGCT: diverting glutamine to glutathione biosynthesis while enhancing glucose anaplerosis for tumor proliferation.Cell death & disease · 2026Article
- Application of the Mass Spectrometry-High-Throughput Technique Over the Immunohistochemical Analysis for Human Brain Tumor Diagnosis and Prognosis: Insights Into Biomarkers' Identification for the Case Study of Grade IV Astrocytomas and Meningiomas.Biomedical chromatography : BMC · 2025Article
- ASAP1 Promotes Epithelial to Mesenchymal Transition by Activating the TGFβ Pathway in Papillary Thyroid Cancer.Cancer medicine · 2025Article
- GGCT participates in the malignant process of hepatocellular cancer cells by regulating the PTEN/PI3K/AKT pathway through binding to EZH2.Discover oncology · 2025Article
- MRPL24 drives breast cancer metastasis and stemness by targeting c-MYC, BRD4, and STAT3.3 Biotech · 2025Article
- Mitochondrial Ribosomal Proteins and Cancer.Medicina (Kaunas, Lithuania) · 2025Review
- Integrated analysis of microbiome and host transcriptome revealed correlations between tissue microbiota and tumor progression in early-stage papillary thyroid carcinoma.Frontiers in cellular and infection microbiology · 2025Article
- Computational-experimental strategy identifies Co-upregulated biomarkers linking coronary heart disease and type 2 diabetes pathogenesis.Frontiers in genetics · 2025Article
- Mechanisms underlying the promotion of papillary thyroid carcinoma occurrence and progression by Hashimoto's thyroiditis.Frontiers in endocrinology · 2025Review
- Mitochondrial ribosomal proteins: potential targets for cancer prognosis and therapy.Frontiers in oncology · 2025Review
- Article
- Identified γ-glutamyl cyclotransferase (GGCT) as a novel regulator in the progression and immunotherapy of pancreatic ductal adenocarcinoma through multi-omics analysis and experiments.Journal of cancer research and clinical oncology · 2024Article
- AEBP1 promotes papillary thyroid cancer progression by activating BMP4 signaling.Neoplasia (New York, N.Y.) · 2024Article
- Development of a thyroid cancer prognostic model based on the mitophagy-associated differentially expressed genes.Discover oncology · 2023Article
- Identification of c-Met as a novel target of γ-glutamylcyclotransferase.Scientific reports · 2023Article
- A cell cycle-related lncRNA signature predicts the progression-free interval in papillary thyroid carcinoma.Frontiers in endocrinology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
Thyroid cancer remains the most common endocrine malignancy worldwide, and its incidence has steadily increased over the past four years. Papillary Thyroid Cancer (PTC) is the most common differentiated thyroid cancer, accounting for 80-85% of all thyroid cancers. Mitochondrial proteins (MRPs) are an important part of the structural and functional integrity of the mitochondrial ribosomal complex. It has been reported that MRPL9 is highly expressed in liver cancer and promotes cell proliferation and migration, but it has not been reported in PTC. In the present study we found that MRPL9 was highly expressed in PTC tissues and cell lines, and lentivirus-mediated overexpression of MRPL9 promoted the proliferation and migration ability of PTC cells, whereas knockdown of MRPL9 had the opposite effect. The interaction between MRPL9 and GGCT (γ-glutamylcyclotransferase) was found by immunofluorescence and co-immunoprecipitation experiments (Co-IP). In addition, GGCT is highly expressed in PTC tissues and cell lines, and knockdown of GGCT/MRPL9 in vivo inhibited the growth of subcutaneous xenografts in nude mice and inhibited the formation of lung metastases. Mechanistically, we found that knockdown of GGCT/MRPL9 inhibited the MAPK/ERK signaling pathway. In conclusion, our study found that the interaction of GGCT and MRPL9 modulates the MAPK/ERK pathway, affecting the proliferation and migration of PTC cells. Therefore, GGCT/MRPL9 may serve as a potential biomarker for PTC monitoring and PTC treatment.
Indexed as
Identifiers
What Socratic holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.