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Roles of Migration and Invasion in Cancer Metastasis
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Roles of Migration and Invasion in Cancer Metastasis

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Oncology".

Deadline for manuscript submissions: 31 December 2024 | Viewed by 1676

Special Issue Editor

Dr. Kyung-Chul Choi

E-Mail Website
Guest Editor
College of Veterinary Medicine, Chungbuk National University, Cheongju 28644, Chungbuk, Republic of Korea
Interests: biochemical toxicology; immunotoxicity; toxic mechanism; cancer biology
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cancer metastasis is the leading cause of cancer-related death in humans. This process is rooted in two steps crucial for cancer cell movement. Migration, the first step, includes the development of cancer within the primary tumor site, whereas invasion, the second step, involves dodging the physical barriers of the body such as blood vessels and the basement membrane to invade the secondary tumor site. Understanding the intricate roles these processes play in metastasis is crucial for developing effective therapies for control or treatment.

Considering the importance of migration and invasion in cancer cell metastasis, the current Special Issue welcomes studies across various disciplines, including:

  • Molecular mechanisms: Analyzing the genetic changes and signaling mechanisms that control adhesion, cytoskeletal dynamics and cell motility.
  • Cellular interactions: Investigating the functions of stromal cells in producing matrix remodeling enzymes, immunological regulators and growth factors that either promote or impede migration and invasion.
  • Clinical implications: Creating novel diagnostic and therapeutic tools that target migration and invasion routes, identifying biomarkers linked to aggressive migration and invasion potential, and evaluating patient data to connect these processes with clinical results.

We invite researchers to contribute their diverse expertise, paving the way for a deeper understanding of this multifaceted process and ultimately, new avenues for combating cancer.

Dr. Kyung-Chul Choi
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • cancer
  • metastasis
  • invasion
  • migration
  • tumor microenviornment
  • epithelial–mesenchymal transition
  • mesenchymal–epithelial transition
  • intravasation
  • extravasation

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Published Papers (1 paper)

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Research

26 pages, 5858 KiB  
Article
A Fungicide, Fludioxonil, Formed the Polyploid Giant Cancer Cells and Induced Metastasis and Stemness in MDA-MB-231 Triple-Negative Breast Cancer Cells
by Ryeo-Eun Go, Su-Min Seong, Youngdong Choi and Kyung-Chul Choi
Int. J. Mol. Sci. 2024, 25(16), 9024; https://doi.org/10.3390/ijms25169024 - 20 Aug 2024
Viewed by 1056
Abstract
Fludioxonil, an antifungal agent used as a pesticide, leaves a measurable residue in fruits and vegetables. It has been identified to cause endocrine disruption, interrupt normal development, and cause various diseases such as cancers. In this study, fludioxonil was examined for its effects [...] Read more.
Fludioxonil, an antifungal agent used as a pesticide, leaves a measurable residue in fruits and vegetables. It has been identified to cause endocrine disruption, interrupt normal development, and cause various diseases such as cancers. In this study, fludioxonil was examined for its effects on the development and metastasis of breast cancer cells. On fludioxonil exposure (10−5 M) for 72 h, mutant p53 (mutp53) MDA-MB-231 triple-negative breast cancer (TNBC) cells significantly inhibited cell viability and developed into polyploid giant cancer cells (PGCCs), with an increase in the number of nuclei and expansion in the cell body size. Fludioxonil exposure disrupted the normal cell cycle phase ratio, resulting in a new peak. In addition, PGCCs showed greater motility than the control and were resistant to anticancer drugs, i.e., doxorubicin, cisplatin, and 5-fluorouracil. Cyclin E1, nuclear factor kappa B (NF-κB), and p53 expressions were remarkably increased, and the expression of cell cycle-, epithelial–mesenchymal-transition (EMT)-, and cancer stemness-related proteins were increased in the PGCCs. The daughter cells obtained from PGCCs had the single nucleus but maintained their enlarged cell size and showed greater cell migration ability and resistance to the anticancer agents. Consequently, fludioxonil accumulated Cyclin E1 and promoted the inflammatory cytokine-enriched microenvironment through the up-regulation of TNF and NF-κB which led to the transformation to PGCCs via abnormal cell cycles such as mitotic delay and mitotic slippage in mutp53 TNBC MDA-MB-231 cells. PGCCs and their daughter cells exhibited significant migration ability, chemo-resistance, and cancer stemness. These results strongly suggest that fludioxonil, as an inducer of potential genotoxicity, may induce the formation of PGCCs, leading to the formation of metastatic and stem cell-like breast cancer cells. Full article
(This article belongs to the Special Issue Roles of Migration and Invasion in Cancer Metastasis)
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