ArticleOncology letters2018
MicroRNA-425 is downregulated in nasopharyngeal carcinoma and regulates tumor cell viability and invasion by targeting hepatoma-derived growth factor.
Article in Oncology letters, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. It has been retracted, and should not be counted. Cited by 7 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
7 citing papers in PubMed, 19 citations in OpenAlex.
- miR-425-5p suppresses tumorigenesis and DDP resistance in human-prostate cancer by targeting GSK3β and inactivating the Wnt/β-catenin signaling pathway.Journal of biosciences · 2019Article
- miR-429 suppresses cell proliferation, migration and invasion in nasopharyngeal carcinoma by downregulation of TLN1.Cancer cell international · 2019Article
- Potential Relationship between Clinical Significance and Serum Exosomal miRNAs in Patients with Multiple Myeloma.BioMed research international · 2019Article
- miR-425 suppresses EMT and the development of TNBC (triple-negative breast cancer) by targeting the TGF-β 1/SMAD 3 signaling pathway.RSC advances · 2018Article
- The regulatory network of nasopharyngeal carcinoma metastasis with a focus on EBV, lncRNAs and miRNAs.American journal of cancer research · 2018Review
- MicroRNA-425-5p Inhibits Lung Cancer Cell GrowthTechnology in cancer research & treatmentArticle
- MicroRNA-425 induces apoptosis and suppresses migration and invasion of human cervical cancer cells by targeting RAB2B.International journal of immunopathology and pharmacologyArticle
Corrections and comments
- Retraction · 2024-01-22Author Unresponsive · Concerns/Issues about Data · Concerns/Issues about Image · Euphemisms for Plagiarism · Investigation by Journal/Publisher · Investigation by Third Party · Paper Mill · Plagiarism of Image · · see also: https://pubpeer.com/publications/C519FEC25F4EB5DC09577338557F97
- Retracted
Authors and funding
4 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nasopharyngeal carcinoma (NPC), which arises from the nasopharynx epithelium, is most common in Southeast Asia, particularly in Southern China. To date, a variety of microRNAs have been demonstrated to serve key functions in the progression and development of NPC. microRNA-425 (miR-425) has previously been reported to be frequently abnormally expressed in a number of different types of human cancer, including lung, gastric, cervical, breast and prostate cancer. However, to the best of our knowledge, the expression patterns, functions and underlying mechanisms of miR-425 in NPC remain largely unexplored. In the present study, the expression of miR-425 was revealed to be low in NPC tissues and cell line. Resumption of miR-425 expression suppressed cell viability and invasion in NPC. Hepatoma-derived growth factor (HDGF) was identified as a direct target gene of miR-425 in NPC. HDGF was highly expressed at mRNA and protein levels in NPC tissues. Additionally, HDGF mRNA was negatively correlated with miR-425 expression in NPC tissues. Furthermore, overexpression of HDGF almost completely rescued the tumor-suppressing effects of miR-425 on NPC cell viability and invasion. Taken together, these results demonstrated that miR-425 acted as a tumor suppressor in NPC by targeting HDGF, suggesting that it may be a novel therapeutic target for the treatments of patients with NPC.
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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.