ArticleBMC pulmonary medicine2022
The LMCD1-AS1/miR-526b-3p/OSBPL5 axis promotes cell proliferation, migration and invasion in non-small cell lung cancer.
Article in BMC pulmonary medicine, 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 It has been retracted, and should not be counted. Cited by 3 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- The miRNA and PD-1/PD-L1 signaling axis: an arsenal of immunotherapeutic targets against lung cancer.Cell death discovery · 2024Review
- miR-526b-5p/c-Myc/Foxp1 participates in recurrent spontaneous abortion by regulating the proliferation, migration, and invasion of trophoblasts.Journal of assisted reproduction and genetics · 2023Article
- The expression, immune infiltration, prognosis, and experimental validation of OSBPL family genes in liver cancer.BMC cancer · 2023Article
Corrections and comments
- Retraction · 2023-08-11Concerns/Issues about Image · Contamination of Cell Lines/Tissues · Error in Image · Unreliable Data · Unreliable Results and/or Conclusions ·
- Retracted
Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
purposeTo explore the specific role and regulatory mechanism of oxysterol binding protein like 5 (OSBPL5) in non-small cell lung cancer (NSCLC). METHODS AND
resultsQuantitative real-time polymerase chain reaction (qRT-PCR) analysis demonstrated that OSBPL5 expression was notably elevated in NSCLC tissues and cell lines, and Kaplan-Meier analysis manifested that high OSBPL5 expression was closely related to the poor prognosis of NSCLC patients. Besides, according to the results from western blot analysis, cell counting kit-8, EdU and Transwell assays, knockdown of OSBPL5 suppressed NSCLC cell proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) process. Additionally, by performing qRT-PCR analysis, luciferase reporter and RNA pull-down assays, we verified that OSBPL5 was a downstream target of miR-526b-3p and long noncoding RNA (lncRNA) LMCD1-AS1 served as a sponge for miR-526b-3p. Moreover, from rescue assays, we observed that OSBPL5 overexpression offset LMCD1-AS1 knockdown-mediated inhibition in cell proliferation, migration, invasion and EMT in NSCLC.
conclusionsThis paper was the first to probe the molecular regulatory mechanism of OSBPL5 involving the LMCD1-AS1/miR-526b-3p axis in NSCLC and our results revealed that the LMCD1-AS1/miR-526b-3p/OSBPL5 axis facilitates NSCLC cell proliferation, migration, invasion and EMT, which may offer a novel therapeutic direction for NSCLC.
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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.