Evidence map›Paper›PMID 42298507›Full record

ArticleBMC cancer2026

In vitro functional analysis of lysyl oxidase family members in highly metastatic pancreatic cancer cells derived from a syngeneic orthotopic model.

Kei Takahashi-Yamashiro, Kensuke Miyauchi, Kazuki Shimomura, Mizuki Nishikawa, Yasuyuki Morishita, Masako Nakanishi, Shinya Hayami, Manabu Kawai, Kohei Miyazono, Shogo Ehata

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in BMC cancer, 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

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

10 authors.

Kei Takahashi-Yamashiro *Department of Molecular Pathology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan.
Kensuke Miyauchi *Department of Molecular Pathology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan.
Kazuki ShimomuraDepartment of Pathology, School of Medicine, Wakayama Medical University, 811-1 Kimiidera, Wakayama-shi, Wakayama, 641-8509, Japan.
Mizuki NishikawaDepartment of Pathology, School of Medicine, Wakayama Medical University, 811-1 Kimiidera, Wakayama-shi, Wakayama, 641-8509, Japan.
Yasuyuki MorishitaDepartment of Molecular Pathology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan.
Masako NakanishiDepartment of Pathology, School of Medicine, Wakayama Medical University, 811-1 Kimiidera, Wakayama-shi, Wakayama, 641-8509, Japan.
Shinya HayamiSecond Department of Surgery, School of Medicine, Wakayama Medical University, 811-1 Kimiidera, Wakayama-shi, Wakayama, 641-8509, Japan.
Manabu KawaiSecond Department of Surgery, School of Medicine, Wakayama Medical University, 811-1 Kimiidera, Wakayama-shi, Wakayama, 641-8509, Japan.
Kohei MiyazonoDepartment of Molecular Pathology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan.
Shogo EhataDepartment of Molecular Pathology, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo, 113-0033, Japan. ehata@wakayama-med.ac.jp.

Funding

Japan Agency for Medical Research Development JP18ck0106193Japan Society for the Promotion of Science JP23H05486Ministry of Education, Culture, Sports, Science and Technology JP17H06326
6 · The paper itself

Abstract

backgroundPancreatic ductal adenocarcinoma (PDAC) is one of the highly lethal malignancies, with no established and effective cure. Therefore, identifying novel molecular targets for this cancer remains an urgent priority. METHODS AND

resultsWe employed a syngeneic orthotopic inoculation model using murine pancreatic cancer Panc02 cells to better recapitulate the pancreatic tumor microenvironment. We established highly metastatic derivatives through three serial transplantation cycles, designated Panc02-3P cells. These cells exhibited enhanced tumorigenicity and metastatic potential both in vitro and in vivo. The RNA-sequence analysis revealed that Panc02-3P cells exhibited mesenchymal-like gene expression changes, compared with parental Panc02 cells, despite no significant changes in EMT-related transcription factor expression. In addition, we found that members of the lysyl oxidase (LOX) family, including LOX, LOXL1, and LOXL3, were markedly upregulated in Panc02-3P cells. The loss-of-function assays using siRNAs targeting LOX and LOXL1 demonstrated that the suppression of these genes significantly attenuated the migratory ability of Panc02-3P cells.

conclusionCollectively, our findings suggest that the LOX family members are associated with the acquisition of a highly migratory and mesenchymal-like phenotype in metastatic pancreatic cancer cells and may contribute to tumor progression.

Indexed as

Carcinoma, Pancreatic DuctalPancreatic NeoplasmsProtein-Lysine 6-OxidaseAnimalsCell Line, TumorCell MovementDisease Models, AnimalEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansMiceNeoplasm MetastasisTumor MicroenvironmentProtein-Lysine 6-OxidaseEMTLysyl oxidase familyMetastasisPancreatic ductal adenocarcinomaSyngeneic orthotopic inoculation model

Identifiers

PMID42298507
PMCPMC13501788

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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.