Evidence map›Paper›PMID 42839997›Full record

ArticleFrontiers in oncology2026

Acidic microenvironment promotes pancreatic cancer cell survival via Akt phosphorylation-mediated suppression of apoptosis.

Raito Yamamoto, Shigekuni Hosogi, Yuki Toda, Atsushi Shiozaki, Eishi Ashihara

Abstract read
In one paragraph

Article in Frontiers in oncology, 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
–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

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.

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

5 authors.

Raito YamamotoLaboratory of Clinical and Translational Physiology, Kyoto Pharmaceutical University, Kyoto, Japan.
Shigekuni HosogiLaboratory of Clinical and Translational Physiology, Kyoto Pharmaceutical University, Kyoto, Japan.
Yuki TodaLaboratory of Clinical and Translational Physiology, Kyoto Pharmaceutical University, Kyoto, Japan.
Atsushi ShiozakiDivision of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Eishi AshiharaLaboratory of Clinical and Translational Physiology, Kyoto Pharmaceutical University, Kyoto, Japan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The microenvironment of many solid tumors is acidic (pH 6.5-6.9) due to hypoxia and enhanced glycolytic metabolism and has been implicated in tumor progression and therapeutic resistance. However, the mechanisms by which pancreatic cancer cells adapt to extracellular acidosis and maintain survival under acidic stress remain incompletely understood. This study aimed to investigate the effects of extracellular acidosis on pancreatic cancer cell proliferation, apoptosis, cell cycle regulation, and intracellular signaling. Human pancreatic cancer cell lines PK-59 and MIA-PaCa-2 were cultured under acidic conditions (pH 6.9). Proliferation, cell cycle phase distribution, apoptosis, and intracellular signaling were assessed using cell growth assays, WST-8 assays, flow cytometry, and western blotting. Pharmacological inhibition of Akt and ERK1/2 was performed to evaluate their functional roles under acidic conditions. Under acidic conditions, both cell lines appeared to show reduced proliferation, an increased G

Indexed as

acidic tumor microenvironmentAKT signalingapoptosisERK1/2 signalingG0/G1 cell cycle delaypancreatic cancer

Identifiers

PMID42839997
PMCPMC13638389

What OpenQuestion holds

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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 OpenQuestion graph.