ArticleJournal of oncology2022
lncRNA TRPM2-AS Promotes Colorectal Cancer Progression by Regulating miR-22-3p and FSTL1.
Article in Journal of oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 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
3 citing papers in PubMed, 9 citations in OpenAlex.
- LncRNA TRPM2-AS promotes cell proliferation, migration, and invasion by regulating the miR-195-5p/COP1 axis in bladder cancer.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- TRPM2-AS promotes ovarian cancer cell proliferation and inhibits cell apoptosis by upregulating the nearby gene TRPM2 via miR-6764-5p.Cell division · 2024Article
- Clinical Significance and Pathogenic Mechanisms of Long Non-Coding RNA TRPM2-AS in Cancers.Technology in cancer research & treatmentReview
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Background: In recent years, long noncoding RNAs (lncRNAs) relate to many biological processes, which affect the progression of tumors. Transient receptor potential melastatin 2 antisense RNA (TRPM2-AS) is reported to play an oncogene-like role in tumors. TRPM2-AS is highly expressed in colorectal cancer (CRC), but the mechanism of TRPM2-AS is still unclear. The regulatory mechanism of TRPM2-AS in the occurrence of CRC was explored, so as to find new markers and therapeutic targets for CRC. Methods: TRPM2-AS and miR-22-3p expression in CRC cells were measured through reverse-transcription quantitative polymerase chain reaction (RT-qPCR). Then, TRPM2-AS knockdown cell lines were constructed, and cell counting kit-8 (CCK-8), clone formation, wound healing, and invasion assays were used to detect cell malignant behavior. Follistatin-like 1 (FSTL1) protein was detected by western blotting. The interaction between miR-22-3p and TRPM2-AS or FSTL1 was verified by the luciferase reporter and RNA immunoprecipitation (RIP) assay. Subcutaneous xenografts were performed using animal experiments. Results: TRPM2-AS expression in CRC cells was increased, and miR-22-3p expression was decreased in CRC cells. TRPM2-AS inhibition inhibited cell malignant behavior. miR-22-3p has a targeting relationship with TRPM2-AS and FSTL1. In cells, downregulation of TRPM2-AS expression promoted miR-22-3p and inhibited FSTL1 expression, while mimics inhibited FSTL1 expression. miR-22-3p inhibition or FSTL1 overexpression could offset the inhibition of TRPM2-AS downregulation on CRC cells. Conclusions: The TRPM2-AS/miR-22-3p/FSTL1 regulation axis could regulate CRC cell malignant behavior, which may provide a new perspective for interpreting the mechanism of CRC development.
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.