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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.
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The mammalian target of rapamycin  (mTOR) is a serine/threonine kinase that regulates growth, proliferation, and cell survival in response to hormones, growth factors, or nutrient availability. This kinase exists in two structurally and functionally distinct forms: mTOR complex 1  (mTORC1) and mTOR complex 2  (mTORC2). The first form (mTORC1) is composed of a rapamycin-sensitive Raptor and proline-rich Akt substrate, PRAS40. In contrast,  mTORC2 consists of a...
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Mitogen-activated protein kinase, or MAPK pathway, activates three sequential kinases to regulate cellular responses such as proliferation, differentiation, survival, and apoptosis. The canonical MAPK pathway starts with a mitogen or growth factor binding to an RTK. The activated RTKs stimulate Ras, which recruits Raf or MAP3 Kinase (MAPKKK), the first kinase of the MAPK signaling cascade. Raf further phosphorylates and activates MEK or MAP2 Kinases (MAPKK), which in turn phosphorylates MAP...
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The Ras-gene-encoded proteins are regulators of signaling pathways controlling cell proliferation, differentiation, or cell survival. The Ras-gene family in humans constitutes three primary members—the HRas, NRas, and KRas. These genes code for four functionally distinct yet closely related proteins—the HRas, NRas, KRas4A, and KRas4B. The involvement of mutant Ras genes in human cancer was first discovered in 1982 and is among the most common causes of human tumorigenesis.
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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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RhoC GTPase Activation Assay
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SMC4 Promotes Prostate Cancer Cell Proliferation and Metastasis via the Rheb/mTOR Pathway.

Wei Zhang1,2, Siyuan Qin3, Xiaokang Li4

  • 1School of Medicine, Southern University of Science and Technology, Shenzhen, Guangdong, 518053, China.

Advanced Science (Weinheim, Baden-Wurttemberg, Germany)
|April 25, 2025
PubMed
Summary
This summary is machine-generated.

Structural maintenance of chromosome protein 4 (SMC4) promotes prostate cancer metastasis by enhancing glycolysis and interacting with GLUT1. Inhibiting SMC4 reduces cancer cell proliferation, migration, and metastasis via the Rheb/mTOR pathway.

Keywords:
GLUT1SMC4metastasisprostate cancer

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Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Prostate cancer metastasis remains a significant clinical challenge.
  • The precise role of Structural Maintenance of Chromosome protein 4 (SMC4) in prostate cancer progression is not fully understood.
  • Aberrant SMC4 expression is linked to metastatic progression in prostate cancer.

Purpose of the Study:

  • To elucidate the functional role of SMC4 in prostate cancer metastasis.
  • To investigate the molecular mechanisms by which SMC4 influences cancer cell behavior.
  • To identify potential therapeutic targets for prostate cancer treatment.

Main Methods:

  • Analysis of The Cancer Genome Atlas (TCGA) database for SMC4 expression patterns.
  • CRISPR/Cas9-mediated SMC4 gene knockdown in RM1-LM cells.
  • In vitro assays for cell proliferation and migration.
  • In vivo murine metastasis model.
  • RNA sequencing (RNA-seq) and KEGG pathway enrichment analysis.
  • Immunoprecipitation-Mass Spectrometry (IP-MS) to identify SMC4 interactors.
  • Co-immunoprecipitation (Co-IP) and glycolytic rate assays.

Main Results:

  • SMC4 knockdown significantly reduced prostate cancer cell proliferation and migration in vitro.
  • SMC4 knockdown diminished lung metastasis capabilities in a murine model.
  • SMC4 knockdown inhibited the Rheb/mTOR signaling pathway and reduced ATP production.
  • SMC4 was found to interact with Glucose Transporter 1 (GLUT1), impacting cellular glycolysis.
  • KEGG analysis revealed enrichment of cancer and metabolic pathways.

Conclusions:

  • SMC4 promotes prostate cancer cell metastasis through interaction with GLUT1 and modulation of the Rheb/mTOR pathway.
  • Targeting SMC4 or its interaction with GLUT1 may represent a novel therapeutic strategy for metastatic prostate cancer.
  • SMC4 plays a critical role in regulating cancer cell metabolism and metastatic potential.