Evidence map›Paper›PMID 41674943›Full record

ArticleTranslational cancer research2026

Sodium selenite promotes apoptosis and augments autophagic flux in cervical cancer cells by activating the YAP-Hippo signaling pathway.

Changhai Wang, Ke Zhu, Long Bai, Xiaoxiao Zhu

Abstract read
In one paragraph

Article in Translational cancer research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing papers in PubMed
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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

The trial behind it

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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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

4 authors.

Changhai Wang *Henan University of Chinese Medicine, Zhengzhou, China.
Ke ZhuHenan University of Chinese Medicine, Zhengzhou, China.
Long BaiChina Academy of Chinese Medical Science, Beijing, China.
Xiaoxiao Zhu *Tianjian Laboratory of Advanced Biomedical Sciences, Academy of Medical Sciences, Zhengzhou University, Zhengzhou, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Selenium (Se) compounds display selective cytotoxicity toward many tumors, yet their activity against cervical cancer is not well-established. This study evaluates the anti-cervical cancer effects of sodium selenite (SS) and clarifies the underlying mechanisms. Methods: HeLa cells were treated with graded SS concentrations. Cell viability was measured using the Cell Counting Kit-8, apoptosis was analyzed by Annexin V/PI flow cytometry, and cell migration and invasion were evaluated by scratch assay and Matrigel-Transwell assay, respectively. Autophagic activity and Hippo signaling were analyzed by Western blotting and immunofluorescence. For Results: SS suppressed HeLa cell proliferation in a concentration- and time-dependent manner [24-h half-maximal inhibitory concentrations (IC Conclusions: SS restrains cervical cancer progression by inducing apoptosis and accelerating autophagosome turnover through activation of the YAP-Hippo axis. These findings highlight SS and YAP-directed modulation in general, as promising avenues for future cervical cancer therapy development.

Indexed as

apoptosisautophagycervical cancerSodium selenite (SS)YAP-Hippo pathway

Identifiers

PMID41674943
PMCPMC12885792

What Socratic holds

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LicenceCC BY-NC-ND
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Registered trials

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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 Socratic graph.