ArticleJournal of oncology2022
Overexpression of LncRNA MNX1-AS1/PPFIA4 Activates AKT/HIF-1
Article in Journal of oncology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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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.
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Who cites it
5 citing papers in PubMed, 6 citations in OpenAlex.
- Targeted Therapy of Tumors and Cancer Stem Cells based on Oxidant-regulated Redox Pathway and its Mechanism.Current computer-aided drug design · 2025Review
- Crosstalk between hypoxia-inducible factor (HIF) and lncRNAs in digestive tumors: from molecular mechanisms to clinical translation.Frontiers in cell and developmental biology · 2025Review
- Long non‑coding RNAs as diagnostic and prognostic biomarkers for colorectal cancer (Review).Oncology letters · 2024Review
- The functions and mechanisms of long non-coding RNA in colorectal cancer.Frontiers in oncology · 2024Review
- Second generation androgen receptor antagonist, TQB3720 abrogates prostate cancer growthFrontiers in pharmacology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: The purpose of this study was to explore the role of the lncRNA MNX1-AS1 and its related downstream signaling pathways in colorectal adenocarcinoma (COAD). Methods: COAD tissues and cells were prepared and treated with sh-MNX1-AS1, pcDNA-MNX1-AS1, sh-PPFIA4, LY29004, and their controls. CCK8 and colony formation assays were undertaken for evaluating cell proliferation. Tumor cell migratory ability was detected by transwell assay. Apoptosis detection was processed by YO-PRO-1/PI Staining. The regulated relationship between lncRNA MNX1-AS1 and PPFIA4 was confirmed by RIP-ChIP assay. Q-PCR was applied to detect genes related to tumor cell stemness, proliferation, migration, and apoptosis in each group. Finally, a xenograft tumor model was constructed to verify the result Results: COAD patients with high expression of the lncRNA MNX1-AS1 have poor prognosis. LncRNA MNX1-AS1 promotes the stemness of COAD cells. PPFIA4 mediates lncRNA MNX1-AS1 expression and affects COAD cell stemness. LncRNA MNX1-AS1 accelerates proliferation and migration, while it suppresses apoptosis. LncRNA MNX1-AS1/PPFIA4 accelerates tumor growth in COAD model. LncRNA MNX1-AS1/PPFIA4 activates the downstream AKT/HIF-1 Conclusion: LncRNA MNX1-AS1/PPFIA4 activates AKT/HIF-1
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.