A type of pancreatic cancer cells form cell clusters from a solitary condition in a primary ciliogenesis-dependent manner.

IF 1.2 4区 医学 Q3 PATHOLOGY
Kenji Shirakawa, Ryota Nakazato, Tetsuhiro Hara, Kenichiro Uemura, Faryal Ijaz, Shinya Takahashi, Koji Ikegami
{"title":"A type of pancreatic cancer cells form cell clusters from a solitary condition in a primary ciliogenesis-dependent manner.","authors":"Kenji Shirakawa, Ryota Nakazato, Tetsuhiro Hara, Kenichiro Uemura, Faryal Ijaz, Shinya Takahashi, Koji Ikegami","doi":"10.1007/s00795-025-00428-0","DOIUrl":null,"url":null,"abstract":"<p><p>Primary cilia are hair-like projections that protrude on most of mammalian cells and mediate reception of extracellular signals. Numerous studies have demonstrated that a variety of cancer cells including pancreatic ductal adenocarcinoma (PDAC) fail to form primary cilia. The loss of primary cilia is thought to cause carcinogenesis and progressive cell proliferation. However, the relationship of the primary cilia loss with carcinogenesis and/or cancer malignancy remains arguable. We herein examined whether ciliogenesis was increased in a model of more progressive PDAC and investigated effects of ciliogenesis on growth of PDAC using a pancreatic cancer cell line, PANC-1. The majority of PANC-1 cells in a cell cluster grown from a solitary cell possessed primary cilia. The rate of ciliogenesis was higher in cells grown from low density than in cells grown from high density. Almost all clones passing limiting dilution culture had abilities to grow primary cilia. Compared to the parental PANC-1 cells, clones that proliferated from a solitary cell showed increase in the ciliogenesis rate. Blocking ciliogenesis suppressed cell cluster formation. Our results suggest that pancreatic cancer cells that are more resistant to a solitary condition have abilities of ciliogenesis and form tumor-like cell clusters in a primary cilia-dependent manner.</p>","PeriodicalId":18338,"journal":{"name":"Medical Molecular Morphology","volume":" ","pages":""},"PeriodicalIF":1.2000,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Medical Molecular Morphology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1007/s00795-025-00428-0","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"PATHOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Primary cilia are hair-like projections that protrude on most of mammalian cells and mediate reception of extracellular signals. Numerous studies have demonstrated that a variety of cancer cells including pancreatic ductal adenocarcinoma (PDAC) fail to form primary cilia. The loss of primary cilia is thought to cause carcinogenesis and progressive cell proliferation. However, the relationship of the primary cilia loss with carcinogenesis and/or cancer malignancy remains arguable. We herein examined whether ciliogenesis was increased in a model of more progressive PDAC and investigated effects of ciliogenesis on growth of PDAC using a pancreatic cancer cell line, PANC-1. The majority of PANC-1 cells in a cell cluster grown from a solitary cell possessed primary cilia. The rate of ciliogenesis was higher in cells grown from low density than in cells grown from high density. Almost all clones passing limiting dilution culture had abilities to grow primary cilia. Compared to the parental PANC-1 cells, clones that proliferated from a solitary cell showed increase in the ciliogenesis rate. Blocking ciliogenesis suppressed cell cluster formation. Our results suggest that pancreatic cancer cells that are more resistant to a solitary condition have abilities of ciliogenesis and form tumor-like cell clusters in a primary cilia-dependent manner.

一种类型的胰腺癌细胞以原发性纤毛发生依赖的方式从孤立状态形成细胞簇。
初级纤毛是在大多数哺乳动物细胞上突出的毛发状突起,介导细胞外信号的接收。大量研究表明,包括胰腺导管腺癌(pancreatic ductal adencarcinoma, PDAC)在内的多种癌细胞不能形成原发性纤毛。原发纤毛的丧失被认为是导致癌变和细胞增殖的原因。然而,原发性纤毛脱落与癌变和/或恶性肿瘤的关系仍有争议。我们在此研究了纤毛发生是否在更进展的PDAC模型中增加,并使用胰腺癌细胞系PANC-1研究了纤毛发生对PDAC生长的影响。在单细胞生长的细胞簇中,大部分的PANC-1细胞具有初级纤毛。低密度培养细胞的纤毛发生率高于高密度培养细胞。几乎所有通过极限稀释培养的无性系都能生长初生纤毛。与亲本PANC-1细胞相比,由单细胞增殖的克隆显示出纤毛发生率的增加。阻断纤毛发生抑制细胞簇的形成。我们的研究结果表明,胰腺癌细胞对孤立条件的抵抗力更强,具有纤毛发生的能力,并以原发性纤毛依赖的方式形成肿瘤样细胞团。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
Medical Molecular Morphology
Medical Molecular Morphology 医学-病理学
CiteScore
2.90
自引率
5.60%
发文量
30
审稿时长
>12 weeks
期刊介绍: Medical Molecular Morphology is an international forum for researchers in both basic and clinical medicine to present and discuss new research on the structural mechanisms and the processes of health and disease at the molecular level. The structures of molecules, organelles, cells, tissues, and organs determine their normal function. Disease is thus best understood in terms of structural changes in these different levels of biological organization, especially in molecules and molecular interactions as well as the cellular localization of chemical components. Medical Molecular Morphology welcomes articles on basic or clinical research in the fields of cell biology, molecular biology, and medical, veterinary, and dental sciences using techniques for structural research such as electron microscopy, confocal laser scanning microscopy, enzyme histochemistry, immunohistochemistry, radioautography, X-ray microanalysis, and in situ hybridization. Manuscripts submitted for publication must contain a statement to the effect that all human studies have been reviewed by the appropriate ethics committee and have therefore been performed in accordance with the ethical standards laid down in an appropriate version of the 1964 Declaration of Helsinki. It should also be stated clearly in the text that all persons gave their informed consent prior to their inclusion in the study. Details that might disclose the identity of the subjects under study should be omitted.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信