ArticleHua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology2022
Oral cancer cells affect pancreatic β-cell function through transmissible endoplasmic reticulum stress.
Article in Hua xi kou qiang yi xue za zhi = Huaxi kouqiang yixue zazhi = West China journal of stomatology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. 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, 0 citations in OpenAlex.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectivesIn this study, we aimed to investigate whether oral cancer cells affect pancreatic β-cells function through transmissible endoplasmic reticulum stress (TERS).
methodsTunicamycin (TM) was selected as the endoplasmic reticulum stress (ERS) inducer. The human oral cancer cell lines CAl-27 and SCC-25 were selected as the donor cells, and mouse insulinoma 6 (MIN6) cell lines were chosen as the recipient cells. Quantitative real-time polymerase chain reaction (qPCR) and Western blot (WB) analysis were used to detect ERS markers and insulin expression. The TdT-mediated dUTP nick-end labeling (TUNEL) method was applied to detect apoptosis levels. The clone formation method was utilized to detect cell proliferation capability. The secretory function of pancreatic β-cells was detected with an enzyme linked immunosorbent assay (ELISA) kit and a bicinchoninic acid (BCA) kit.
resultsThe MIN6 cells were subjected to TM stimulation. qPCR and WB analysis revealed that ERS markers were upregulated. This result implied that the MIN6 cells can induce ERS. The supernatant of oral cancer cells under ERS was added to the MIN6 cells. qPCR and WB analysis showed that the oral cancer cells that had been subjected to ERS could induce ERS in the MIN6 cells, that is, the phenomenon of TERS occurred. The TUNEL assay indicated that the apoptosis of the MIN6 cells increased under TERS. The clone formation assay demonstrated that the proliferation capability of the MIN6 cells decreased under TERS. qPCR and WB analysis revealed that under TERS, insulin synthesis by the MIN6 cells decreased and insulin synthesis was inhibited at the translation level. The ELISA and BCA kits demonstrated that insulin secretion by the MIN6 cells was reduced under TERS.
conclusionsOral cancer cells can affect pancreatic β-cells through TERS, resulting in increased apoptosis, decreased viability, and reduced insulin secretion and synthesis capability.
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.