LncRNA NUTM2A‐AS1 positively modulates TET1 and HIF‐1A to enhance gastric cancer tumorigenesis and drug resistance by sponging miR‐376a
Open accessAbstract
Long noncoding RNA NUTM2A‐AS1 has been shown to be dysregulated in non‐small cell lung carcinoma. To date, it is unclear whether NUTM2A‐AS1 plays a role in gastric cancer progression. The purpose of this study is to elucidate the molecular mechanism of the role of NUTM2A‐AS1 in gastric cancer. mRNA and protein levels were measured by RT‐qPCR and western blot methods. Invasion ability was examined by transwell assay. Cell viability was determined by MTT assay. Dual‐luciferase assay, RNA pull down, and RNA immunoprecipitation were used to confirm direct binding of between miR‐376a and NUTM2A‐AS1 or TET1. Xenografting tumor assay and TCGA analysis showed the contributory role of NUTM2A‐AS1 in vivo and human clinical setting. Our results suggested that NUTM2A‐AS1 promoted cell viability, invasion, and drug resistance of gastric cancer cells, which was largely rescued by miR‐376a. More interestingly, TET1 and HIF‐1A were negatively regulated by miR‐376a. TET1 could interact with HIF‐1A to modulate PD‐L1. Finally, we revealed that PD‐L1 was key to NUTM2A‐AS1‐ and miR‐376a‐mediated tumorigenesis and drug resistance. In summary, our conclusions facilitate us understand the underlying mechanism and develop novel treatment strategy for gastric cancer.
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Integrity signals
Registry
Cites
Statistics
Claims the paper makes
The claims and statistics of this paper haven’t been checked yet.
Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.
Claims other papers make about this one
Each is checked against this paper’s own text: does it say what the citing paper says it does?
Various critical transcription factors, including HIF-1α, c-MYC, NF-kB, STAT3, c-JUN, and miR-138-5p, have been shown to transcriptionally regulate PD-L1 expression.
“Various critical transcription factors, including HIF-1α, c-MYC, NF-kB, STAT3, c-JUN, and miR-138-5p have been shown to transcriptionally regulate PD-L1 expression25–30.”
From PRDM1/BLIMP1 induces cancer immune evasion by modulating the USP22-SPI1-PD-L1 axis in hepatocellular carcinoma cells (2022) · cites this paper as [25]
The Results section ('TET1 interacts with HIF-1A to regulate PD-L1'; page unavailable) reports that HIF-1A enhanced PD-L1 expression in gastric cancer cells. The copy does not establish PD-L1 regulation by the other listed factors—c-MYC, NF-kB, STAT3, c-JUN, or miR-138-5p—so it supports only the HIF-1α part of the sentence. (LLM, conf=0.88)
Experimental — accuracy not yet measured
Self-check
Percentages, sums and reported differences re-computed from the paper’s own numbers.
The self-check needs the paper’s full text.
The citation lists haven’t been fetched yet
References 39 · Cited by 54
- Authors
- Wang, J., Yu, Z., Wang, J., Shen, Y., Qiu, J., & Zhuang, Z.
- Affiliations
- Second Affiliated Hospital of Soochow University (CN)
- Suzhou Science and Technology Town Hospital (CN)
- Corresponding author
- Zhuang, Zhixiang
- Venue
- Cancer Medicine
- Publisher
- Wiley
- Published
- 2020-10-22
- Volume
- 9
- Issue
- 24
- Pages
- 9499-9510
- ISSN
- 2045-7634 (ISSN-L)
- PMC
- PMC7774746
- OpenAlex
- W3093607399
- Cited by
- 54
- References
- 39
- Citations by year
- 2026: 3 · 2025: 9 · 2024: 13 · 2023: 9 · 2022: 12 · 2021: 8
- FWCI
- 2.48
- Type
- journal article
- Language
- en
- Open access
- gold
- doi.org
- Licence
- Locations
- Cancer Medicine (publishedVersion, cc-by)
- Europe PMC (PubMed Central) (publishedVersion, other-oa)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- Funders
- National Natural Science Foundation of China (81603181)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer-related molecular mechanisms research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › MicroRNA in disease regulation
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › RNA modifications and cancer
- Keywords
- long non-coding RNA, miR-376a, TET1, HIF1A, PD-L1, gastric cancer, drug resistance, carcinogenesis, cell invasion, microRNA sponge
- MeSH terms
- Animals, Cell Movement, Humans, Mixed Function Oxygenases, Proto-Oncogene Proteins, Stomach Neoplasms, Survival Rate, Mice, SCID, Mice, Inbred NOD, Apoptosis, Drug Resistance, Neoplasm, Databases, Genetic, MicroRNAs, Cell Line, Tumor, Cell Proliferation, Mice, Hypoxia-Inducible Factor 1, alpha Subunit, B7-H1 Antigen, RNA, Long Noncoding, Heterografts
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
Are you an author, or do you see a problem with this page? Request a review