ArticleOncology reports2020
Long non‑coding RNA LINC00858 promotes TP53‑wild‑type colorectal cancer progression by regulating the microRNA‑25‑3p/SMAD7 axis.
Article in Oncology reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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
5 citing papers in PubMed, 13 citations in OpenAlex.
- Article
- Roles of TGF‑β signalling pathway‑related lncRNAs in cancer (Review).Oncology letters · 2023Review
- LINC00858 promotes colon cancer progression through activation of STAT3/5 signaling by recruiting transcription factor RAD21 to upregulate PCNP.Cell death discovery · 2022Article
- Upregulated miRNAs on theFrontiers in genetics · 2022Article
- Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long non‑coding RNAs (lncRNAs) are involved in colorectal cancer (CRC) progression, however the mechanisms remain largely unknown. The present study aimed to reveal the role and possible molecular mechanisms of a new LNCRNA, LINC00858, in CRC. LINC00858 was increased in CRC tumor tissues, and patients with high LINC00858 expression had a shorter survival time. Knockdown of LINC00858 expression suppressed cell proliferation and induced G0/G1 cell cycle arrest and apoptosis in TP53‑wild‑type CRC cells. Subsequently, using Starbase v2.0 database, miR‑25‑3p was confirmed to interact with LINC00858 and was downregulated by LINC00858. Reduction of miR‑25‑3p expression with an inhibitor significantly attenuated the biological effects of LINC00858 knockdown in CRC cells. Furthermore, using TargetScan, SMAD7 was validated to interact with miR‑25‑3p and was downregulated by miR‑25‑3p. Lastly, the ectopic overexpression of SMAD7 rescued the suppressive effects of LINC00858 knockdown in CRC cells. Collectively, the results from the present study, to the best of our knowledge, firstly demonstrated a novel LINC00858/miR‑25‑3p/SMAD7 regulatory axis that promoted CRC progression, indicating LINC00858 as a promising therapeutic target for CRC.
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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.