ArticleExperimental and therapeutic medicine2020
SNHG1 promotes proliferation, migration and invasion of bladder cancer cells via the PI3K/AKT signaling pathway.
Article in Experimental and therapeutic medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 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
9 citing papers in PubMed, 15 citations in OpenAlex.
- Research progress on the role of AGC kinase family in bladder cancer.Discover oncology · 2025Review
- Unlocking the life code: a review of SnoRNA functional diversity and disease relevance.Cell communication and signaling : CCS · 2025Review
- microRNA 21 and long non-coding RNAs interplays underlie cancer pathophysiology: A narrative review.Non-coding RNA research · 2024Review
- LncRNA SNHG1: role in tumorigenesis of multiple human cancers.Cancer cell international · 2023Review
- SNHG1 functions as a ceRNA in hypertrophic scar fibroblast proliferation and apoptosis through miR-320b/CTNNB1 axis.Archives of dermatological research · 2023Article
- The long and short non-coding RNAs modulating EZH2 signaling in cancer.Journal of hematology & oncology · 2022Review
- LncSNHG1 Promoted CRC Proliferation through the miR-181b-5p/SMAD2 Axis.Journal of oncology · 2022Article
- Long non-coding RNA SNHG1 promotes bladder cancer progression by upregulating EZH2 and repressing KLF2 transcription.Clinics (Sao Paulo, Brazil) · 2022Article
- Hypoxic Breast Cancer Cell-Derived Exosomal SNHG1 Promotes Breast Cancer Growth and Angiogenesis via Regulating miR-216b-5p/JAK2 Axis.Cancer management and research · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Long non-coding RNA (lncRNA) small nucleolar RNA host gene 1 (SNHG1) has been previously reported to mediate a number of functions during the progression of cancer. However, its involvement in bladder cancer remain unclear. The aim of the present study was to investigate the expression of SNHG1 in bladder cancer and to identify its potential mechanisms. SNHG1 expression was firstly detected in cancer tissues and cells. The effects of SNHG1 on the malignant phenotypes were then investigated. Furthermore, the influence of SNHG1 on the PI3K/AKT signaling pathway was examined. It was demonstrated that SNHG1 expression was significantly upregulated in bladder cancer tissues and cells. Moreover, the loss-of-function experimental results suggested that knockdown of SNHG1 inhibited bladder cancer cell proliferation, migration and invasion, but increased apoptosis; however, SNHG1 overexpression promoted these processes. Mechanistically, rescue assays identified that SNHG1 activated the PI3K/AKT signaling pathway. Therefore, it was speculated that SNHG1 functioned as a carcinogenic lncRNA in bladder cancer via activation of PI3K/AKT.
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.