Evidence map›Paper›PMID 39819714›Full record

ArticleNan fang yi ke da xue xue bao = Journal of Southern Medical University2025

Inhibiting miR-155-5p promotes proliferation of human submandibular gland epithelial cells in primary Sjogren's syndrome by negatively regulating the PI3K/AKT signaling pathway

Yuru Zhang, Lei Wan, Haoxiang Fang, Fangze Li, Liwen Wang, Kefei Li, Peiwen Yan, Hui Jiang

Abstract read
In one paragraph

Article in Nan fang yi ke da xue xue bao = Journal of Southern Medical University, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors.

Yuru ZhangFirst Affiliated Hospital of Anhui University of Traditional Chinese Medicine, Hefei 230031, China.
Lei WanFirst Affiliated Hospital of Anhui University of Traditional Chinese Medicine, Hefei 230031, China.
Haoxiang FangCollege of Traditional Chinese Medicine, Anhui University of Traditional Chinese Medicine, Hefei 230031, China.
Fangze LiFirst Affiliated Hospital of Anhui University of Traditional Chinese Medicine, Hefei 230031, China.
Liwen WangFirst Affiliated Hospital of Anhui University of Traditional Chinese Medicine, Hefei 230031, China.
Kefei LiFirst Affiliated Hospital of Anhui University of Traditional Chinese Medicine, Hefei 230031, China.
Peiwen YanFirst Affiliated Hospital of Anhui University of Traditional Chinese Medicine, Hefei 230031, China.
Hui JiangFirst Affiliated Hospital of Anhui University of Traditional Chinese Medicine, Hefei 230031, China.

Funding

National Natural Science Foundation of China 82474482 and 82274501
6 · The paper itself

Abstract

objectivesTo investigate the mechanism mediating the regulatory effect of miR-155-5p on proliferation of human submandibular gland epithelial cells (HSGECs) in primary Sjogren's syndrome (pSS).

methodsDual luciferase reporter assay was used to verify the targeting relationship between miR-155-5p and the PI3K/AKT pathway. In a HSGEC model of pSS induced by simulation with TRAIL and INF-γ, the effects of miR-155-inhibitor-NC or miR-155 inhibitor on cell viability, cell cycle, apoptosis and proliferation were evaluated using CKK8 assay, flow cytometry and colony formation assay. ELISA and RT-PCR were used to detect the expressions of inflammatory cytokines and miR-155-5p mRNA in the cells; Western blotting was performed to detect the expressions of proteins in the PI3K/AKT signaling pathway.

resultsDual luciferase assay showed that miR-155-5p targets the PI3K/AKT pathway via PIK3R1 mRNA. The HSGEC model of pSS showed significantly decreased cell viability, cell clone formation ability and expressions IL-10 and IL-4 and increased cell apoptosis, cell percentage in G2 phase, expressions of TNF‑α, IL-6, miR-155-5p and PIK3R1 mRNA, p-PI3K/PI3K ratio, p-Akt/AKT ratio, and PIK3R1 protein expression. Treatment of the cell models with miR-155 inhibitor significantly increased the cell viability, G1 phase cell percentage, colony formation ability, and expressions of IL-10 and IL-4 levels, and obviously reduced cell apoptosis rate, G2 phase cell percentage, expressions of TNF-α, IL-6, miR-155-5p and PIK3R1 mRNA, p-PI3K/PI3K ratio, p-AKT/AKT ratio, and PIK3R1 protein expression.

conclusionsIn HSGEC model of pSS, inhibition of miR-155-5p can promote cell proliferation and reduced cell apoptosis by targeting PI3K1 mRNA to negatively regulate the overexpression of PI3K/AKT signaling pathway.

Indexed as

Epithelial CellsMicroRNAsSjogren's SyndromeApoptosisCell ProliferationCells, CulturedClass Ia Phosphatidylinositol 3-KinaseHumansPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktSignal TransductionSubmandibular GlandClass Ia Phosphatidylinositol 3-KinaseMicroRNAsMIRN155 microRNA, humanPhosphatidylinositol 3-KinasesPIK3R1 protein, humanProto-Oncogene Proteins c-aktinflammatory factorsmiR-155-5pPI3K/AKT signaling pathwayPIK3R1primary Sjogren's syndrome

Identifiers

PMID39819714
PMCPMC11744292

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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.