Evidence map›Paper›PMID 32535957›Full record

ArticleCancer science2020

Cancer-associated adipocytes promote pancreatic cancer progression through SAA1 expression.

Masanori Takehara, Yasushi Sato, Tetsuo Kimura, Kazuyoshi Noda, Hiroshi Miyamoto, Yasuteru Fujino, Jinsei Miyoshi, Fumika Nakamura, Hironori Wada, Yoshimi Bando and 4 more

Open access · goldAbstract read
In one paragraph

Article in Cancer science, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 1 pooled it
6.1field-weighted citation impact, top 3% of its field
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

71 citing papers in PubMed, 1 synthesis or guideline pooled it, 125 citations in OpenAlex.

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11 more citing papers are in PubMed but not listed here.

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

14 authors at 3 institutions in 1 country.

Masanori TakeharaDepartment of Gastroenterology and Oncology, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima City, Japan.ORCID https://orcid.org/0000-0002-9024-4900
Yasushi SatoDepartment of Gastroenterology and Oncology, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima City, Japan.
Tetsuo KimuraDepartment of Gastroenterology and Oncology, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima City, Japan.
Kazuyoshi NodaDepartment of Gastroenterology and Oncology, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima City, Japan.
Hiroshi MiyamotoDepartment of Gastroenterology and Oncology, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima City, Japan.
Yasuteru FujinoDepartment of Gastroenterology and Oncology, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima City, Japan.
Jinsei MiyoshiDepartment of Gastroenterology and Oncology, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima City, Japan.
Fumika NakamuraDepartment of Gastroenterology and Oncology, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima City, Japan.
Hironori WadaDepartment of Gastroenterology and Oncology, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima City, Japan.
Yoshimi BandoDivision of Pathology, Tokushima University Hospital, Tokushima City, Japan.
Tetsuya IkemotoDepartment of Surgery, Institute of Health Biosciences, Tokushima University Graduate School, The University of Tokushima, Tokushima City, Japan.
Mitsuo ShimadaDepartment of Surgery, Institute of Health Biosciences, Tokushima University Graduate School, The University of Tokushima, Tokushima City, Japan.
Naoki MugurumaDepartment of Gastroenterology and Oncology, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima City, Japan.
Tetsuji TakayamaDepartment of Gastroenterology and Oncology, Institute of Biomedical Sciences, Tokushima University Graduate School, Tokushima City, Japan.ORCID https://orcid.org/0000-0002-0175-1573
Tokushima University · JPKochi Rehabilitation Institute · JPTokushima University Hospital · JP

Funding

Japan Society for the Promotion of Science JP19K17464
6 · The paper itself

Abstract

Although pancreatic cancer often invades peripancreatic adipose tissue, little information is known about cancer-adipocyte interaction. We first investigated the ability of adipocytes to de-differentiate to cancer-associated adipocytes (CAAs) by co-culturing with pancreatic cancer cells. We then examined the effects of CAA-conditioned medium (CAA-CM) on the malignant characteristics of cancer cells, the mechanism underlying those effects, and their clinical relevance in pancreatic cancer. When 3T3-L1 adipocytes were co-cultured with pancreatic cancer cells (PANC-1) using the Transwell system, adipocytes lost their lipid droplets and changed morphologically to fibroblast-like cells (CAA). Adipocyte-specific marker mRNA levels significantly decreased but those of fibroblast-specific markers appeared, characteristic findings of CAA, as revealed by real-time PCR. When PANC-1 cells were cultured with CAA-CM, significantly higher migration/invasion capability, chemoresistance, and epithelial-mesenchymal transition (EMT) properties were observed compared with control cells. To investigate the mechanism underlying these effects, we performed microarray analysis of PANC-1 cells cultured with CAA-CM and found a 78.5-fold higher expression of SAA1 compared with control cells. When the SAA1 gene in PANC-1 cells was knocked down with SAA1 siRNA, migration/invasion capability, chemoresistance, and EMT properties were significantly attenuated compared with control cells. Immunohistochemical analysis on human pancreatic cancer tissues revealed positive SAA1 expression in 46/61 (75.4%). Overall survival in the SAA1-positive group was significantly shorter than in the SAA1-negative group (P = .013). In conclusion, we demonstrated that pancreatic cancer cells induced de-differentiation in adipocytes toward CAA, and that CAA promoted malignant characteristics of pancreatic cancer via SAA1 expression, suggesting that SAA1 is a novel therapeutic target in pancreatic cancer.

Indexed as

3T3 CellsAdipocytesAdultAgedAged, 80 and overAnimalsCell DedifferentiationCell Line, TumorCell ProliferationCoculture TechniquesCulture Media, ConditionedDisease-Free SurvivalDisease ProgressionEpithelial-Mesenchymal TransitionFemaleFollow-Up StudiesCulture Media, ConditionedRNA, Small InterferingSAA1 protein, humanSerum Amyloid A Proteincancer-associated adipocytescancer microenvironmentmetastasispancreatic cancerSAA1

Identifiers

PMID32535957
PMCPMC7419047
OpenAlexW3034999789

What OpenQuestion holds

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LicenceCC BY-NC
Read underepoch 390

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.