Evidence map›Paper›PMID 38536483›Full record

ArticleJournal of gastroenterology2024

CACNA2D1 regulates the progression and influences the microenvironment of colon cancer.

Hiroyuki Inoue, Atsushi Shiozaki, Toshiyuki Kosuga, Hiroki Shimizu, Michihiro Kudou, Tomohiro Arita, Hirotaka Konishi, Shuhei Komatsu, Yoshiaki Kuriu, Takeshi Kubota and 4 more

Open access · hybridAbstract read
PubMed Publisher
In one paragraph

Article in Journal of gastroenterology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed
1.4field-weighted citation impact, top 20% 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

7 citing papers in PubMed, 6 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Calcium channels as pharmacological targets for cancer therapy.Clinical and experimental medicine · 2025
    Review
  6. Extracellular matrix stiffness regulates colorectal cancer progression via HSF4.Journal of experimental & clinical cancer research : CR · 2025
    Article
  7. Article
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 1 institution in 1 country.

Hiroyuki Inoue *Division of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, 465 Kajii-Cho, Kamigyo-Ku, Kyoto, 602-8566, Japan.
Atsushi Shiozaki *Division of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, 465 Kajii-Cho, Kamigyo-Ku, Kyoto, 602-8566, Japan. shiozaki@koto.kpu-m.ac.jp.ORCID 0000-0003-3739-160X
Toshiyuki KosugaDivision of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, 465 Kajii-Cho, Kamigyo-Ku, Kyoto, 602-8566, Japan.
Hiroki ShimizuDivision of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, 465 Kajii-Cho, Kamigyo-Ku, Kyoto, 602-8566, Japan.
Michihiro KudouDivision of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, 465 Kajii-Cho, Kamigyo-Ku, Kyoto, 602-8566, Japan.
Tomohiro AritaDivision of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, 465 Kajii-Cho, Kamigyo-Ku, Kyoto, 602-8566, Japan.
Hirotaka KonishiDivision of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, 465 Kajii-Cho, Kamigyo-Ku, Kyoto, 602-8566, Japan.
Shuhei KomatsuDivision of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, 465 Kajii-Cho, Kamigyo-Ku, Kyoto, 602-8566, Japan.
Yoshiaki KuriuDivision of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, 465 Kajii-Cho, Kamigyo-Ku, Kyoto, 602-8566, Japan.
Takeshi KubotaDivision of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, 465 Kajii-Cho, Kamigyo-Ku, Kyoto, 602-8566, Japan.
Hitoshi FujiwaraDivision of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, 465 Kajii-Cho, Kamigyo-Ku, Kyoto, 602-8566, Japan.
Yukiko MorinagaDepartment of Surgical Pathology, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Eiichi KonishiDepartment of Surgical Pathology, Kyoto Prefectural University of Medicine, Kyoto, Japan.
Eigo OtsujiDivision of Digestive Surgery, Department of Surgery, Kyoto Prefectural University of Medicine, 465 Kajii-Cho, Kamigyo-Ku, Kyoto, 602-8566, Japan.
Kyoto Prefectural University of Medicine · JP

Funding

Japan Society for the Promotion of Science 21K08689Japan Society for the Promotion of Science 22K08832Japan Society for the Promotion of Science 22K16518Japan Society for the Promotion of Science 23K06654Japan Society for the Promotion of Science 23K08115Japan Society for the Promotion of Science 23K08218
6 · The paper itself

Abstract

backgroundCalcium voltage-gated channel auxiliary subunit alpha 2/delta 1 (CACNA2D1), a gene encoding a voltage-gated calcium channel, has been reported as an oncogene in several cancers. However, its role in colon cancer (CC) remains unclear. This study aimed to investigate the function of CACNA2D1 and its effect on the microenvironment in CC.

methodsImmunohistochemistry (IHC) analysis was performed on samples collected from 200 patients with CC who underwent curative colectomy. Knockdown experiments were performed using CACNA2D1 siRNA in the human CC cell lines HCT116 and RKO, and cell proliferation, cycle, apoptosis, and migration were then analyzed. The fibroblast cell line CCD-18Co was co-cultured with CC cell lines to determine the effect of CACNA2D1 on fibroblasts and the relationship between CACNA2D1 and the cancer microenvironment. Gene expression profiles of cells were analyzed using microarray analysis.

resultsIHC revealed that high CACNA2D1 expression was an independent poor prognostic factor in patients with CC and that CACNA2D1 expression and the stroma are correlated. CACNA2D1 depletion decreased cell proliferation and migration; CACNA2D1 knockdown increased the number of cells in the sub-G1 phase and induced apoptosis. CCD-18Co and HCT116 or RKO cell co-culture revealed that CACNA2D1 affects the cancer microenvironment via fibroblast regulation. Furthermore, microarray analysis showed that the p53 signaling pathway and epithelial-mesenchymal transition-associated pathways were enhanced in CACNA2D1-depleted HCT116 cells.

conclusionsCACNA2D1 plays an important role in the progression and the microenvironment of CC by regulating fibroblasts and may act as a biomarker for disease progression and a therapeutic target for CC.

Indexed as

ApoptosisCalcium ChannelsColonic NeoplasmsDisease ProgressionTumor MicroenvironmentAgedCell Line, TumorCell MovementCell ProliferationCoculture TechniquesEpithelial-Mesenchymal TransitionFemaleFibroblastsGene Expression Regulation, NeoplasticGene Knockdown TechniquesHCT116 CellsCACNA2D1 protein, humanCalcium ChannelsCACNA2D1Colon cancerFibroblastp53Voltage-gated calcium channel

Identifiers

PMID38536483
OpenAlexW4393220092

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.