ArticleMolecular medicine reports2018
miR‑3666 suppresses cellular proliferation and invasion in colorectal cancer by targeting SATB2.
Article in Molecular medicine reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 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
8 citing papers in PubMed, 10 citations in OpenAlex.
- Advances in research on SATB2 and its role in tumor development.Cell & bioscience · 2025Review
- Reduced Expression of SATB2 in Colorectal Cancer and Its Association with Demographic and Clinicopathological Parameters.International journal of molecular sciences · 2025Article
- Comprehensive Computational Assessment of SNAI1 and SNAI2 in Gastric Cancer: Linking EMT, Tumor Microenvironment, and Survival Outcomes.Cancer informatics · 2025Article
- Circ_0008315 promotes tumorigenesis and cisplatin resistance and acts as a nanotherapeutic target in gastric cancer.Journal of nanobiotechnology · 2024Article
- Expression status of circ-SMARCA5, circ-NOL10, circ-LDLRAD3, and circ-RHOT1 in patients with colorectal cancer.Scientific reports · 2023Article
- EphA3 targeted by miR-3666 contributes to melanoma malignancy via activating ERK1/2 and p38 MAPK pathways.Open medicine (Warsaw, Poland) · 2022Article
- SATB2: A versatile transcriptional regulator of craniofacial and skeleton development, neurogenesis and tumorigenesis, and its applications in regenerative medicine.Genes & diseases · 2022Review
- Function and mechanisms of microRNA-20a in colorectal cancer.Experimental and therapeutic medicine · 2020Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
MicroRNA‑3666 (miR‑3666) acts as a tumor suppressor in cervical cancer, non‑small cell lung cancer and thyroid carcinoma; however, the function of miR‑3666 in colorectal cancer (CRC) remains largely unknown. In the present study, was demonstrated that miR‑3666 was significantly downregulated in CRC tissues compared with in adjacent normal tissues by reverse transcription‑quantitative polymerase chain reaction. Additionally, miR‑3666 may serve as a prognostic biomarker for patients with CRC. Via functional experiments, the present study reported that miR‑3666 overexpression significantly inhibited the proliferation, migration and invasion of CRC cells as determined by Cell Counting Kit‑8 and Transwell assays, and vice versa. In addition, miR‑3666 was reported to directly target special AT‑rich sequence binding protein 2 (SATB2) in CRC cells; overexpression of miR‑3666 significantly suppressed the expression of SATB2 in CRC cells as determined by western blotting. Furthermore, an inverse correlation was observed between the expression levels of miR‑3666 and SATB2 in CRC tissues. Restoration of SATB1 expression significantly reversed the effects of miR‑3666 mimic on CRC cells. In summary, the results of the present study indicated that miR‑3666 may serve as a tumor suppressor in CRC by targeting SATB2.
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.