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Molecular Research in Prostate Cancer

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 May 2025 | Viewed by 607

Special Issue Editor


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Guest Editor
Center for Cancer Research and Therapeutic Development, Clark Atlanta University, 223 James P. Brawley Dr., Atlanta, GA 30314, USA
Interests: prostate cancer; cell signaling; cell proliferation; cell migration/invasion
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

The focus of the Special Issue will be on changes in cell signaling mechanisms that are involved in cell proliferation, migration, and invasion in prostate cancer cells during different stages of cancer progression. For example, TGFβ signaling plays critical roles during different stages of prostate cancer development. In the earlier stages of cancer development, TGFβ acts as a tumor suppressor by inhibiting cell proliferation and maintaining differentiation. In the later stages, the cancer cells develop resistance to these inhibitory effects of TGFβ on cell proliferation while maintaining the other components of TGFβ signaling. In these cells, TGFβ acts as a tumor promoter by inducing epithelial to mesenchymal transformation (EMT), cell migration, invasion and metastasis, and immune suppression. The cellular and molecular mechanisms involved in these varied effects of TGFβ are not fully understood. These mechanisms may involve reorganization and/or alterations of intracellular signaling cascades during different stages of cancer progression, resulting in altered cellular responses. This Special Issue will focus on these and other similar signaling pathways that may be altered and play differential roles during different stages of prostate cancer development and progression.

Prof. Dr. Shafiq Khan
Guest Editor

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Keywords

  • cell proliferation
  • cell migration and invasion
  • metastasis
  • growth factor
  • TGFβ
  • cell signaling

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Published Papers (1 paper)

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Research

10 pages, 1851 KiB  
Article
i2 Induces Cell Migration in PC3 Prostate Cancer Cells in the Absence of Rac1 Activation
by Rarnice Johnson, Silvia Caggia and Shafiq A. Khan
Int. J. Mol. Sci. 2025, 26(6), 2663; https://doi.org/10.3390/ijms26062663 - 15 Mar 2025
Viewed by 486
Abstract
Metastatic prostate cancer occurs when the tumor spreads from the prostate gland to other parts of the body. Previous studies have shown that Gαi2, a subunit of the heterotrimeric G protein complex, plays a critical role in inducing cell migration and [...] Read more.
Metastatic prostate cancer occurs when the tumor spreads from the prostate gland to other parts of the body. Previous studies have shown that Gαi2, a subunit of the heterotrimeric G protein complex, plays a critical role in inducing cell migration and invasion in prostate cancer cells in response to diverse stimuli. Rac1 is a small rho-GTPase, which is activated by the phosphoinositide 3-kinase (PI3K)/AKT pathway and plays an essential role during cell migration. Previous studies have shown that the knockdown of Gαi2 attenuates cell migration without causing any reduction in basal Rac1 activity in both PC3 and DU145 cells, and has only marginal effects on the epidermal growth facotor (EGF)-induced increase in Rac1 activity. Therefore, Gαi2 may be involved in the regulation of cell motility and invasion independently or downstream of Rac1 activation. In this study, we investigated the possible mechanism of Gαi2 at the level of the Rac1-dependent activation of Wiskott-Aldrich Syndrome Protein)-family verprolin homologous protein2 (Wave2) and actin related protein 2/3 (Arp 2/3) proteins, downstream effectors of activated Rac1. PC3 cells with a stable overexpression of constitutively active Rac1 were transfected with control siRNA or Gαi2 siRNA to knockdown endogenous Gαi2 expression. Western blot analysis showed that the Rac1-dependent activation of Wave2 was impaired in the absence of Gαi2. The overexpression of constitutively active Gαi2 (Gαi2-Q205L) in PC3 cells significantly increased cell migration compared to cells transfected with control plasmids. In the parallel experiments, a specific Gαi2 inhibitor blocked Giα2-Q205L-induced cell migration in PC3 cells. Furthermore, the Rac1 inhibitor did not block increased cell migration in PC3 cells overexpressing constitutively active Gαi2. We conclude that activated Gαi2 plays a crucial role in cell migration in prostate cancer cells independent of Rac1 activation. Full article
(This article belongs to the Special Issue Molecular Research in Prostate Cancer)
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