ArticleWorld journal of gastroenterology2013
Underexpression of LATS1 TSG in colorectal cancer is associated with promoter hypermethylation.
Article in World journal of gastroenterology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 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
33 citing papers in PubMed, 61 citations in OpenAlex.
- WWP2 drives the progression of gastric cancer by facilitating the ubiquitination and degradation of LATS1 protein.Cell communication and signaling : CCS · 2023Article
- Investigation of the Effects of Apigenin, a Possible Therapeutic Agent, on Cytotoxic and SWH Pathway in Colorectal Cancer (HT29) Cells.Advanced pharmaceutical bulletin · 2023Article
- Tumor suppressor genes are reactivated by miR-26A1 via enhancer reprogramming in NSCLC.Human molecular genetics · 2023Article
- The clinicopathological and prognostic significances of LATS1 expression in breast cancer.Histology and histopathology · 2022Article
- Article
- Guidelines for accreditation of endoscopy units: quality measures from the Korean Society of Coloproctology.Annals of surgical treatment and research · 2021Article
- SHANK2 is a frequently amplified oncogene with evolutionarily conserved roles in regulating Hippo signaling.Protein & cell · 2021Article
- Epigenetic Regulation of the Wnt/β-Catenin Signaling Pathway in Cancer.Frontiers in genetics · 2021Review
- LATS1 exerts tumor suppressor functions via targeting Gli1 in colorectal cancer.Journal of Cancer · 2021Article
- [Emerging roles of Hippo signaling pathway in gastrointestinal cancers and its molecular mechanisms].Zhejiang da xue xue bao. Yi xue ban = Journal of Zhejiang University. Medical sciences · 2020Review
- Promoter Hypermethylation of LATS2 Gene in Oral Squamous Cell Carcinoma (OSCC) Among North Indian Population.Asian Pacific journal of cancer prevention : APJCP · 2020Article
- Immunohistochemical Profile of Tumor Suppressor Proteins RASSF1A and LATS1/2 in Relation to p73 and YAP Expression, of Human Inflammatory Bowel Disease and Normal Intestine.Pathology oncology research : POR · 2020Article
- Distinct Expression Patterns of Two Tumor Necrosis Factor Superfamily Member 15 Gene Isoforms in Human Colon Cancer.Digestive diseases and sciences · 2019Article
- Overexpression of lncRNA PIK3CD-AS1 promotes expression of LATS1 by competitive binding with microRNA-566 to inhibit the growth, invasion and metastasis of hepatocellular carcinoma cells.Cancer cell international · 2019Article
- RASAL2 promotes tumor progression through LATS2/YAP1 axis of hippo signaling pathway in colorectal cancer.Molecular cancer · 2018Article
- Molecular Alterations and Expression Dynamics of LATS1 and LATS2 Genes in Non-Small-Cell Lung Carcinoma.Pathology oncology research : POR · 2018Article
- LATS1 inhibits metastasis and epithelial-mesenchymal transition in head and neck squamous cell carcinoma.International journal of clinical and experimental pathology · 2018Article
- MethylatedOncotarget · 2017Article
- miR-21 inhibition of LATS1 promotes proliferation and metastasis of renal cancer cells and tumor stem cell phenotype.Oncology letters · 2017Article
- The LATS1 and LATS2 tumor suppressors: beyond the Hippo pathway.Cell death and differentiation · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
12 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo investigate large tumor suppressor 1 (LATS1) expression, promoter hypermethylation, and microsatellite instability in colorectal cancer (CRC).
methodsRNA was isolated from tumor tissue of 142 CRC patients and 40 colon mucosal biopsies of healthy controls. After reverse transcription, quantitative polymerase chain reaction (PCR) was performed, and LATS1 expression was normalized to expression of the ACTB and RPL32 housekeeping genes. To analyze hypermethylation, genomic DNA was isolated from 44 tumor CRC biopsies, and methylation-specific PCR was performed. Microsatellite instability (MSI) status was checked with PCR using BAT26, BAT25, and BAT40 markers in the genomic DNA of 84 CRC patients, followed by denaturing gel electrophoresis.
resultsDecreased LATS1 expression was found in 127/142 (89.4%) CRC cases with the average ratio of the LATS1 level 10.33 ± 32.64 in CRC patients vs 32.85 ± 33.56 in healthy controls. The lowest expression was found in Dukes' B stage tumors and G1 (well-differentiated) cells. Hypermethylation of the LATS1 promoter was present in 25/44 (57%) CRC cases analyzed. LATS1 promoter hypermethylation was strongly associated with decreased gene expression; methylated cases showed 162× lower expression of LATS1 than unmethylated cases. Although high-grade MSI (mutation in all three markers) was found in 14/84 (17%) cases and low-grade MSI (mutation in 1-2 markers) was found in 30/84 (36%) cases, we found no association with LATS1 expression.
conclusionDecreased expression of LATS1 in CRC was associated with promoter hypermethylation, but not MSI status. Such reduced expression may promote progression of CRC.
Indexed as
Identifiers
What OpenQuestion 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 OpenQuestion graph.