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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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Genes usually encode proteins necessary for the proper functioning of a healthy cell. Mutations can often cause changes to the gene expression pattern, thereby altering the phenotype.
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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.
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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 orderly progression of the cell cycle depends on the activation of Cdk protein by binding to its cyclin partner. However, the cell cycle must be restricted when undergoing abnormal changes. Most cancers correlate to the deregulated cell cycle, and since Cdks are a central component of the cell cycle, Cdk inhibitors are extensively studied to develop anticancer agents. For instance, cyclin D associates with several Cdks, such as Cdk 4/6, to form an active complex. The cyclin D-Cdk4/6 complex...
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Author Spotlight: Exploring Salidroside's Molecular Mechanisms in Breast Cancer Treatment
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CDCA2 Promotes HCC Cells Development via AKT-mTOR Pathway.

Kai Li1,2, Tingting Fan1, Zhongxing Shi1

  • 1Department of Radiology, The Second Affiliated Hospital of Harbin Medical University, Harbin 150001, China.

Analytical Cellular Pathology (Amsterdam)
|January 2, 2023
PubMed
Summary
This summary is machine-generated.

Cell division cycle associated 2 (CDCA2) promotes hepatocellular carcinoma (HCC) growth and spread. Targeting CDCA2 may offer a new strategy for treating this aggressive cancer by influencing the AKT-mTOR pathway.

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Area of Science:

  • Oncology
  • Molecular Biology

Background:

  • Hepatocellular carcinoma (HCC) is an aggressive malignancy with poor patient prognosis.
  • Cell division cycle associated 2 (CDCA2) is overexpressed in HCC and linked to patient outcomes.
  • The specific role and mechanism of CDCA2 in HCC remain to be fully elucidated.

Purpose of the Study:

  • To investigate the functional role of CDCA2 in HCC cells.
  • To explore the underlying molecular mechanism by which CDCA2 influences HCC progression.

Main Methods:

  • Gain- and loss-of-function experiments were performed on HCC cells.
  • Quantitative reverse transcription-polymerase chain reaction and Western blot assessed CDCA2 mRNA and protein levels.
  • Cell viability, colony formation, migration, and invasion assays evaluated malignant behaviors. Western blot also analyzed the AKT-mTOR pathway and Cyclin D1 expression.

Main Results:

  • CDCA2 expression was significantly increased in HCC cell lines.
  • Upregulation of CDCA2 enhanced HCC cell growth, migration, and invasion, while depletion had opposite effects.
  • CDCA2 upregulation correlated with increased levels of phosphorylated AKT (p-AKT), phosphorylated mTOR (p-mTOR), and Cyclin D1, which decreased upon CDCA2 depletion.

Conclusions:

  • CDCA2 significantly promotes the malignant progression of HCC cells.
  • The AKT-mTOR signaling pathway is implicated in the mechanism by which CDCA2 drives HCC development.