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Related Concept Videos

Cancer Stem Cells and Tumor Maintenance02:40

Cancer Stem Cells and Tumor Maintenance

Early diagnosis and treatment can often cure cancer. However, even with treatment, residual cells called cancer stem cells (CSC) might remain, often causing tumor recurrence. These cancer stem cells possess the potential for self-renewal and multi-lineage differentiation and are often responsible for the therapeutic resistance displayed in most cancers.
Cancer stem cells are thought to originate from tissue-specific normal stem cells or progenitor cells. The normal stem cells usually reside in...
Cancer Stem Cells and Tumor Maintenance02:40

Cancer Stem Cells and Tumor Maintenance

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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...
mTOR Signaling and Cancer Progression03:03

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M-Cdk Drives Transition Into Mitosis02:15

M-Cdk Drives Transition Into Mitosis

Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
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M-Cdk Drives Transition Into Mitosis02:15

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Checkpoints throughout the cell cycle serve as safeguards and gatekeepers, allowing the cell cycle to progress in favorable conditions and slow or halt it in problematic ones. This regulation is known as the cell cycle control system.
Cyclin-dependent kinases, or Cdks, work in concert with cyclins to control cell cycle transitions. M-Cdk, a complex of Cdk1 bound to M cyclin, is a well-known example of this coordinated control that drives the transition from the G2 to the M phase.
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Related Experiment Video

Updated: Jun 25, 2026

Isolation of Cancer Stem Cells From Human Prostate Cancer Samples
07:16

Isolation of Cancer Stem Cells From Human Prostate Cancer Samples

Published on: March 14, 2014

METTL3/YTHDF1-Driven SURF6 Promotes Prostate Cancer Stemness via CDK4.

Yue Cheng1, Min Zhang1, Danfang Shi1

  • 1Department of Clinical Laboratory, Tongde Hospital of Zhejiang Province, Hangzhou, China.

Journal of Cellular and Molecular Medicine
|June 24, 2026
PubMed
Summary
This summary is machine-generated.

SURF6 gene is upregulated in prostate cancer (PCa), promoting tumor growth and spread. Targeting SURF6 could offer a new therapeutic strategy for PCa patients.

Keywords:
CDK4PCaSURF6m6A modificationproliferation

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Last Updated: Jun 25, 2026

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Area of Science:

  • Oncology
  • Molecular Biology
  • Cancer Genetics

Background:

  • Prostate cancer (PCa) presents a significant global health burden.
  • Novel therapeutic targets are crucial for improving PCa patient outcomes.
  • Understanding the molecular drivers of PCa progression is essential.

Purpose of the Study:

  • To investigate the role of the SURF6 gene in prostate cancer.
  • To elucidate the molecular mechanisms underlying SURF6's function in PCa.
  • To evaluate SURF6 as a potential therapeutic target for PCa.

Main Methods:

  • Bioinformatics analysis and gene expression profiling.
  • Western blotting and functional assays (proliferation, migration, invasion, stemness).
  • In vitro and in vivo (xenograft) studies to assess SURF6 modulation effects.

Main Results:

  • SURF6 is significantly upregulated in PCa tissues, correlating with poor prognosis.
  • SURF6 silencing inhibits PCa cell proliferation, migration, and invasion.
  • SURF6 regulates CDK4 expression and cancer stem cell markers (CD44, Nanog).
  • METTL3 and YTHDF1 regulate SURF6 via m6A modification.
  • SURF6 knockdown inhibits tumor growth and stemness in vivo.

Conclusions:

  • SURF6 plays a critical role in promoting prostate cancer progression.
  • SURF6 is a potential therapeutic target for improving PCa treatment strategies.
  • Targeting SURF6 may offer a novel approach for clinical intervention in PCa.