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Cancers
Special Issues
Cell Migration and Invasion in Cancer
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Cell Migration and Invasion in Cancer

A special issue of Cancers (ISSN 2072-6694). This special issue belongs to the section "Molecular Cancer Biology".

Deadline for manuscript submissions: 28 February 2025 | Viewed by 1606

Special Issue Editor

Prof. Dr. Suresh K Alahari

E-Mail Website
Guest Editor
Department of Biochemistry and Molecular Biology, LSU School of Medicine, New Orleans, LA 70112, USA
Interests: cell adhesion; Nischarin; tumor cell migration; invasion; microRNA; lncRNA
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Cell invasion and migration play important roles in embryonic development, homeostasis, and pathobiology and the process of cancer progression. Cell migration is coordinated by a plethora of cytoplasmic proteins which involve a transient signaling event with changes in the cellular architecture. In cancer progression, tumor cells originate from their primary site and metastasize to the distant organ. Various cytoplasmic protein and transcription factors have been identified to mediate this process. The progression of cancer to metastasis is a major reason for cancer death. In this Special Issue, we will briefly describe the role of various tumor suppressors, oncogenes, miRNA, and their targets in the regulation of tumor cell invasion, migration, and metastasis in different forms of cancer.

Prof. Dr. Suresh K Alahari
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 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. Cancers is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). 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

  • cell migration
  • invasion
  • tumor
  • metastasis
  • genes
  • microRNA

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Published Papers (2 papers)

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Research

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13 pages, 4724 KiB  
Article
MicroRNA-532-3p Modulates Colorectal Cancer Cell Proliferation and Invasion via Suppression of FOXM1
by Ketakee Mahajan, Ani V. Das, Suresh K. Alahari, Ramesh Pothuraju and S. Asha Nair
Cancers 2024, 16(17), 3061; https://doi.org/10.3390/cancers16173061 - 2 Sep 2024
Viewed by 1067
Abstract
Colorectal cancer (CRC) is a heterogeneous disease and classified into various subtypes, among which transcriptional alterations result in CRC progression, metastasis, and drug resistance. Forkhead-box M1 (FOXM1) is a proliferation-associated transcription factor which is overexpressed in CRC and the mechanisms of FOXM1 regulation [...] Read more.
Colorectal cancer (CRC) is a heterogeneous disease and classified into various subtypes, among which transcriptional alterations result in CRC progression, metastasis, and drug resistance. Forkhead-box M1 (FOXM1) is a proliferation-associated transcription factor which is overexpressed in CRC and the mechanisms of FOXM1 regulation have been under investigation. Previously, we showed that FOXM1 binds to promoters of certain microRNAs. Database mining led to several microRNAs that might interact with FOXM1 3’UTR. The interactions between shortlisted microRNAs and FOXM1 3’UTR were quantitated by a dual-luciferase reporter assay. MicroRNA-532-3p interacted with the 3’UTR of the FOXM1 mRNA transcript most efficiently. MicroRNA-532-3p was ectopically overexpressed in colorectal cancer (CRC) cell lines, leading to reduced transcript and protein levels of FOXM1 and cyclin B1, a direct transcriptional target of FOXM1. Further, a clonogenic assay was conducted in overexpressed miR-532-3p CRC cells that revealed a decline in the ability of cells to form colonies and a reduction in migratory and invading potential. These alterations were reinforced at molecular levels by the altered transcript and protein levels of the conventional EMT markers E-cadherin and vimentin. Overall, this study identifies the regulation of FOXM1 by microRNA-532-3p via its interaction with FOXM1 3’UTR, resulting in the suppression of proliferation, migration, and invasion, suggesting its role as a tumor suppressor in CRC. Full article
(This article belongs to the Special Issue Cell Migration and Invasion in Cancer)
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Review

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25 pages, 1477 KiB  
Review
Impact of Radiation on Invasion and Migration of Glioma In Vitro and In Vivo
by Marina Santiago Franco, Susanne Raulefs, Daniela Schilling, Stephanie E. Combs and Thomas E. Schmid
Cancers 2024, 16(23), 3900; https://doi.org/10.3390/cancers16233900 - 21 Nov 2024
Viewed by 174
Abstract
Glioblastoma (GBM) constitutes the most common primary brain tumor and it remains incurable despite therapeutic advances. The high infiltration/invasion potential of GBM cells is considered to be one of the reasons for the inevitable recurrence of the disease. Radiotherapy (RT) is part of [...] Read more.
Glioblastoma (GBM) constitutes the most common primary brain tumor and it remains incurable despite therapeutic advances. The high infiltration/invasion potential of GBM cells is considered to be one of the reasons for the inevitable recurrence of the disease. Radiotherapy (RT) is part of the standard care for patients with GBM, and its benefits on overall survival are extensively reported. However, numerous preclinical studies show that X-ray irradiation can enhance the motility of GBM cells. In the present review, we bring together state-of-the-art research on the impact of radiation on GBM cell motility. The mechanisms through which irradiation impacts the brain tumor microenvironment and the tumor cells themselves, leading to more aggressive/invasive tumors, are described. Finally, we summarize potential pharmacological strategies to overcome this problem. Clinical data validating the occurrence of these processes are urgently needed as they could be of great value for patient outcomes. With this comprehensive review, we expect to highlight the need for methods which allow for monitoring the post-irradiation invasive behavior of GBM in patients. Full article
(This article belongs to the Special Issue Cell Migration and Invasion in Cancer)
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Planned Papers

The below list represents only planned manuscripts. Some of these manuscripts have not been received by the Editorial Office yet. Papers submitted to MDPI journals are subject to peer-review.

Title: Molecular insights of signaling cascade in breast cancer: A Comprehensive Review
Authors: Venketesh K. Panda; Barnalee Mishra; Samikshya Mahapatra; Biswajit Swain; Diksha Malhotra; Suryendu Saha; Sinjan Khanra; Priyanka Mishra; Sambhunath Majhi; Kavita Kumari; Angitha N Nath; Swarnali Saha; Sarmistha Jena; Gopal C. Kundu
Affiliation: KIIT University
Abstract: The complex signaling network within the breast tumor microenvironment (TME) is crucial for its growth, metastasis, angiogenesis, therapy escape, stem cell maintenance, and immunomodulation. An array of secretory factors and their receptors activate downstream signaling cascades regulating breast cancer progression and metastasis. Among various signaling pathways, the epidermal growth factor receptors (EGFR), estrogen receptor (ER), Notch, and hedgehog signaling pathways have recently been identified to exert a crucial function in breast cancer proliferation, survival, differentiation, and maintenance of CSCs and therapy failure. These receptors mediate various downstream signaling pathways such as MAPK, Ras/Raf/MEK/ERK, PI3K/Akt, Wnt/β-catenin, and JAK/STAT. Additionally, these cascades orchestrate intricate interplay between stromal cells, immune cells, and tumor cells. Metabolic reprogramming and adaptations contribute to aggressive breast cancer and are unresponsive to therapy. Herein, the recent insights into the novel signaling pathways operating within the breast TME that aid in their advancement have been emphasized. Current developments in practices aimed at targeting breast TME to enhance treatment efficacy have been reviewed.

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