Evidence map›Paper›PMID 42663874›Full record

ArticleMolecular and cellular biochemistry2026

Lactic acid exposure alters lysophosphatidic acid receptor-mediated regulation of growth and motility in pancreatic cancer cells.

Mao Yamamoto, Miwa Takai, Nanami Shimomura, Eiki Isa, Narumi Yashiro, Moemi Tamura, Shion Nagano, Yuka Kusumoto, Toshifumi Tsujiuchi

Abstract read
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In one paragraph

Article in Molecular and cellular biochemistry, 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

9 authors.

Mao Yamamoto *Division of Molecular Oncology, Department of Life Science, Faculty of Science and Engineering, Kindai University, 3-4-1, Kowakae, Higashiosaka, Osaka, 577-8502, Japan.
Miwa Takai *Division of Molecular Oncology, Department of Life Science, Faculty of Science and Engineering, Kindai University, 3-4-1, Kowakae, Higashiosaka, Osaka, 577-8502, Japan.
Nanami ShimomuraDivision of Molecular Oncology, Department of Life Science, Faculty of Science and Engineering, Kindai University, 3-4-1, Kowakae, Higashiosaka, Osaka, 577-8502, Japan.
Eiki IsaDivision of Molecular Oncology, Department of Life Science, Faculty of Science and Engineering, Kindai University, 3-4-1, Kowakae, Higashiosaka, Osaka, 577-8502, Japan.
Narumi YashiroDivision of Molecular Oncology, Department of Life Science, Faculty of Science and Engineering, Kindai University, 3-4-1, Kowakae, Higashiosaka, Osaka, 577-8502, Japan.
Moemi TamuraDivision of Molecular Oncology, Department of Life Science, Faculty of Science and Engineering, Kindai University, 3-4-1, Kowakae, Higashiosaka, Osaka, 577-8502, Japan.
Shion NaganoDivision of Molecular Oncology, Department of Life Science, Faculty of Science and Engineering, Kindai University, 3-4-1, Kowakae, Higashiosaka, Osaka, 577-8502, Japan.
Yuka KusumotoDivision of Molecular Oncology, Department of Life Science, Faculty of Science and Engineering, Kindai University, 3-4-1, Kowakae, Higashiosaka, Osaka, 577-8502, Japan.
Toshifumi TsujiuchiDivision of Molecular Oncology, Department of Life Science, Faculty of Science and Engineering, Kindai University, 3-4-1, Kowakae, Higashiosaka, Osaka, 577-8502, Japan. ttujiuch@life.kindai.ac.jp.

Funding

Japan Society for the Promotion of Science 21K07109
6 · The paper itself

Abstract

Lysophosphatidic acid (LPA) receptor signaling contributes to the regulation of cancer cell functions. Lactic acid serves not only as an important energy source for cancer cells but also activates various signaling pathways that influence cancer cell behavior. To investigate the roles of LPA receptors in the malignant behavior of pancreatic cancer PANC-1 cells, PANC-LA1 and PANC-LA5 cells were generated by culturing PANC-1 cells with 1 or 5 mM lactic acid, respectively, for approximately 3 months. LPAR1, LPAR3, and LPAR5 expression levels expression levels were elevated, whereas LPAR2 expression was reduced in PANC-LA1 and PANC-LA5 cells compared with PANC-1 cells. PANC-1 cell growth was inhibited by LPA. Conversely, PANC-LA1 cell growth remained unchanged in response to LPA, and LPA increased PANC-LA5 cell growth. The motility of PANC-LA1 and PAN-LA5 cells was markedly elevated compared with that of PANC-1 cells. LPA further enhanced PANC-LA1 and PAN-LA5 cell motility but did not affect PANC-1 cell motility. In the presence of LPA, AM966 inhibited, whereas TC LPA5 4 stimulated PANC-LA5 cell growth and PANC-LA1 cell motility. Although GRI-977,143 increased PANC-LA5 cell growth, it reduced PANC-LA1 cell motility. (2S)-OMPT increased PANC-LA5 cell growth and PANC-LA1 cell motility. When cells were cultured in serum-free media, the viability of PANC-LA1 and PANC-LA5 cells was higher compared with that of PANC-1 cells. PANC-LA5 cell growth and PANC-LA1 cell motility were inhibited by AZD3965 and galloflavin. These findings indicate that LPA receptor signaling is involved in the regulation of PANC-1 cell behavior induced by long-term lactic acid exposure, with LPA

Indexed as

Cellular functionsLactic acidLPA receptorsLysophosphatidic acidPancreatic cancer cells

Identifiers

PMID42663874

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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.