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Related Concept Videos

mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

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The mammalian target of rapamycin or mTOR protein was discovered in 1994 due to its direct interaction with rapamycin. The protein gets its name from a yeast homolog called TOR. The mTOR protein complex in mammalian cells plays a major role in balancing anabolic processes such as the synthesis of proteins, lipids, and nucleotides and catabolic processes, such as autophagy in response to environmental cues, such as availability of nutrients and growth factors.
The mTOR pathway or the...
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Role of Myosin in Cell Migration01:18

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Myosins are multimeric motor proteins involved in various cellular processes such as migration, adhesion, and proliferation. Myosin II is the most common type in animal cells, which binds and cross-links actin filaments.
Myosin II  is a hexamer comprising two heavy chains with globular heads and coiled-coil tails, two regulatory light chains, and two essential light chains. The ATPase sites on the myosin heads hydrolyze ATP, and the released phosphate generates the force for contraction....
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Abnormal Proliferation02:23

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Under normal conditions, most adult cells remain in a non-proliferative state unless stimulated by internal or external factors to replace lost cells. Abnormal cell proliferation is a condition in which the cell's growth exceeds and is uncoordinated with normal cells. In such situations, cell division persists in the same excessive manner even after cessation of the stimuli, leading to persistent tumors. The tumor arises from the damaged cells that replicate to pass the damage to the...
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The Tumor Microenvironment02:17

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Every normal cell or tissue is embedded in a complex local environment called stroma, consisting of different cell types, a basal membrane, and blood vessels. As normal cells mutate and develop into cancer cells, their local environment also changes to allow cancer progression. The tumor microenvironment (TME) consists of a complex cellular matrix of stromal cells and the developing tumor. The cross-talk between cancer cells and surrounding stromal cells is critical to disrupt normal tissue...
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Cancer Cell Migration through Invadopodia01:35

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Invadosome is a broad category of cell surface structures with proteolytic activity that  degrades the extracellular matrix (ECM). Invadosomes are present in normal cell types, including macrophages, endothelial cells, and neurons, as well as tumor cells. Although the macrophage podosomes and tumor cell invadopodia are classified as invadosomes, they have different structures, molecular pathways, and functions. Podosomes are short structures that last for a few minutes. However,...
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Mitogens and the Cell Cycle02:38

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Mitogens and their receptors play a crucial role in controlling the progression of the cell cycle. However, the loss of mitogenic control over cell division leads to tumor formation. Therefore, mitogens and mitogen receptors play an important role in cancer research. For instance, the epidermal growth factor (EGF) - a type of mitogen and its transmembrane receptor (EGFR), decides the fate of the cell's proliferation. When EGF binds to EGFR, a member of the ErbB family of tyrosine kinase...
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  5. Biomedical And Clinical Sciences
  7. Oncology And Carcinogenesis
  9. Predictive And Prognostic Markers
  11. Myo6 Contributes To Tumor Progression And Enzalutamide Resistance In Castration-resistant Prostate Cancer By Activating The Focal Adhesion Signaling Pathway.
  1. Home
  3. Research Domains
  5. Biomedical And Clinical Sciences
  7. Oncology And Carcinogenesis
  9. Predictive And Prognostic Markers
  11. Myo6 Contributes To Tumor Progression And Enzalutamide Resistance In Castration-resistant Prostate Cancer By Activating The Focal Adhesion Signaling Pathway.

Related Experiment Video

Characterization of Cell Membrane Extensions and Studying Their Roles in Cancer Cell Adhesion Dynamics
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Characterization of Cell Membrane Extensions and Studying Their Roles in Cancer Cell Adhesion Dynamics

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MYO6 contributes to tumor progression and enzalutamide resistance in castration-resistant prostate cancer by activating the focal adhesion signaling pathway.

Shengfeng Zheng1,2,3,4, Zhe Hong5,6,7, Yao Tan1,2,8

  • 1Department of Urology, Fudan University Shanghai Cancer Center, Shanghai, 200032, China.

Cell Communication and Signaling : CCS
|October 25, 2024

View abstract on PubMed

Summary
This summary is machine-generated.
Keywords:
Androgen receptorCastration-resistant prostate cancerEnzalutamide resistanceMyosin VI

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Myosin VI (MYO6) promotes castration-resistant prostate cancer (CRPC) progression and enzalutamide (Enz) resistance by activating the AR/MYO6/FAK pathway. Targeting MYO6 may offer a new therapeutic strategy for Enz-resistant CRPC.

Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Research

Background:

  • Enzalutamide (Enz) resistance is a significant challenge in treating castration-resistant prostate cancer (CRPC).
  • Aberrant androgen receptor (AR) expression is a common mechanism in CRPC.
  • Myosin VI (MYO6) is implicated in cell survival and is upregulated in prostate cancer (PCa).

Purpose of the Study:

  • To investigate the role of MYO6 in Enz resistance in CRPC.
  • To elucidate the underlying molecular mechanisms of MYO6-mediated Enz resistance.
  • To explore MYO6 as a potential therapeutic target for Enz-resistant CRPC.

Main Methods:

  • Analysis of open-access databases for MYO6 expression and PCa progression.
  • In vitro and in vivo tumorigenesis assays to assess MYO6 function.
Y15
  • Investigation of AR binding to the MYO6 promoter and FAK activation.
  • Utilized human PCa tissues and clinical data.

    • Main Results:

    • MYO6 expression correlates positively with AR expression in PCa.
    • AR directly upregulates MYO6 transcription, promoting PCa cell proliferation, migration, invasion, and inhibiting apoptosis.
    • MYO6 activates FAK phosphorylation via ITGB8 modulation, driving PCa progression and Enz resistance.
    • Knockdown of MYO6 resensitizes CRPC cells to Enz treatment.
    • FAK inhibition by Y15 resensitizes CRPC cells to Enz therapy.

    Conclusions:

    • MYO6 exhibits pro-tumorigenic and Enz-resistant properties in CRPC.
    • The AR/MYO6/FAK signaling pathway is crucial for Enz resistance.
    • Targeting MYO6 presents a promising therapeutic strategy for Enz-resistant CRPC.