ArticleBioengineered2022
SNF5 promotes cell proliferation and immune evasion in non-small cell lung cancer.
Article in Bioengineered, 2022. 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 It has been retracted, and should not be counted. Not yet cited in PubMed.
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
0 citing papers in PubMed, 1 citations in OpenAlex.
No citing paper in PubMed yet.
Corrections and comments
- Retracted
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immune evasion is the process that tumor cells accelerate growth and metastasis by evading the recognition and attack of immune cells. SNF5 is one of the core subunits of SWI/SNF, which is involved in the development of a variety of malignancies. However, the functions of SNF5 in Non-Small Cell Lung Cancer (NSCLC) and the mechanism of SNF5 regulates immune evasion are still unclear. Based on this, we analyzed the expression of SNF5 and overall survival of lung cancer tissues through the cancer genome atlas (TCGA) database. Then we performed genetic gain and loss of function experiments with SNF5 using lentivirus infection and siRNA in NSCLC A549 and NCI-H1299 cells, respectively. We investigated the proliferation and immune evasion of these cells. We further explored the mechanism of SNF5 on NSCLC cells immune evasion. Our data showed that SNF5 was significantly increased in lung cancer tissues than that in normal lung tissues. Furthermore, SNF5 promoted NSCLC cells proliferation and the expressions of immune evasion-related genes. Meantime, overexpressed SNF5 reduced mortality of A549 cells when co-cultured with T cells. Moreover, SNF5 regulated the immune evasion by activating the signal transducer and activator of transcription (STAT3)/ phospho-STAT3 pathway in NSCLC cells. Together, our results validate SNF5 as a tumor oncogene and provide a new target for NSCLC treatment.
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.