Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

4.7K
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...
4.7K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

3.8K
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...
3.8K
The Retinoblastoma Gene01:20

The Retinoblastoma Gene

4.1K
Tumor suppressor genes are normal genes that can slow down cell division, repair DNA mistakes, or program the cells for apoptosis in case of irreparable damage. Hence, they play an essential role in preventing the proliferation of damaged cells.
The first-ever tumor suppressor gene called Rb was identified in retinoblastoma - a rare eye tumor in children. In inherited forms of the disease, a child inherits one defective copy of the Rb gene, which predisposes them to retinoblastoma. However,...
4.1K
Interactions Between Signaling Pathways01:19

Interactions Between Signaling Pathways

6.3K
Signaling cascades usually lack linearity. Multiple pathways interact and regulate one another, allowing cells to integrate and respond to diverse environmental stimuli.
Convergence and divergence, and cross-talk between signaling pathways
Two distinct signaling pathways can converge on a single functional unit, which may either be a single protein or a complex of proteins. The response is either functionally distinct or synergistic between the two pathways but different from the response...
6.3K
Cancer-Critical Genes II: Tumor Suppressor Genes01:05

Cancer-Critical Genes II: Tumor Suppressor Genes

7.4K
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.
When the function of certain critical genes, especially those involved in cell cycle regulation and cell growth signaling cascades, gets disrupted, it upsets the cell cycle progression. Such cells with unchecked cell cycles start proliferating uncontrollably and eventually develop into tumors.
Such genes that act...
7.4K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

3.5K
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...
3.5K
  1. Home
  2. Circ-ip6k2 Suppresses Tumor Progression By Modulating The Mir-1292-5p/camk2n1 Signal In Clear Cell Renal Cell Carcinoma.
  1. Home
  2. Circ-ip6k2 Suppresses Tumor Progression By Modulating The Mir-1292-5p/camk2n1 Signal In Clear Cell Renal Cell Carcinoma.

Related Experiment Video

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
11:44

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis

Published on: March 30, 2019

7.6K

Circ-IP6K2 suppresses tumor progression by modulating the miR-1292-5p/CAMK2N1 signal in clear cell renal cell

Jian-Ying Tang1, Lu Yang1, Qing-Jian Wu2

  • 1Department of Nephrology, University-Town Hospital of Chongqing Medical University, No 55 road of University-Town, Shapingba District, Chongqing, 401331, P.R. China.

Functional & Integrative Genomics
|July 9, 2024

View abstract on PubMed

Summary
This summary is machine-generated.

Circular RNA circ-IP6K2 is downregulated in clear cell renal cell carcinoma (ccRCC), suppressing tumor growth and progression. It acts by sponging miR-1292-5p, impacting the CAMK2N1 tumor suppressor and the β-catenin/c-Myc pathway.

Keywords:
CAMK2N1Circ-IP6K2Clear cell renal cell carcinomaProgressionmiR-1292-5p

More Related Videos

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
00:07

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

Published on: August 23, 2019

7.3K
Modeling Spontaneous Metastatic Renal Cell Carcinoma mRCC in Mice Following Nephrectomy
11:27

Modeling Spontaneous Metastatic Renal Cell Carcinoma mRCC in Mice Following Nephrectomy

Published on: April 29, 2014

16.6K

Related Experiment Videos

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis
11:44

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis

Published on: March 30, 2019

7.6K
In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice
00:07

In Vivo Inhibition of MicroRNA to Decrease Tumor Growth in Mice

Published on: August 23, 2019

7.3K
Modeling Spontaneous Metastatic Renal Cell Carcinoma mRCC in Mice Following Nephrectomy
11:27

Modeling Spontaneous Metastatic Renal Cell Carcinoma mRCC in Mice Following Nephrectomy

Published on: April 29, 2014

16.6K

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Renal cell carcinoma (RCC), particularly the clear cell subtype (ccRCC), presents a significant clinical challenge due to its aggressive nature and poor prognosis.
  • Circular RNAs (circRNAs) are emerging as key regulators in tumorigenesis, but their specific roles in ccRCC remain largely undefined.

Purpose of the Study:

  • To investigate the role of circ-IP6K2 in the development and progression of clear cell renal cell carcinoma.
  • To elucidate the molecular mechanisms underlying circ-IP6K2's function in ccRCC.

Main Methods:

  • Analysis of circRNA expression in ccRCC tissues using the GSE100186 dataset.
  • In vitro assays to assess the effects of circ-IP6K2 on cell proliferation, migration, and invasion.
  • In vivo xenograft models to evaluate tumor growth inhibition.
  • Mechanistic studies involving RNA immunoprecipitation and luciferase reporter assays to identify circRNA-miRNA-mRNA interactions.
  • Main Results:

    • Circ-IP6K2 was significantly downregulated in ccRCC tissues, with decreased expression correlating with advanced TNM stage, higher histological grade, and poorer overall survival.
    • Overexpression of circ-IP6K2 suppressed ccRCC cell proliferation, migration, and invasion in vitro, and inhibited tumor growth in vivo.
    • Circ-IP6K2 functioned as a molecular sponge for miR-1292-5p, leading to the upregulation of its target gene, CAMK2N1.
    • CAMK2N1, a tumor suppressor, negatively regulated the oncogenic β-catenin/c-Myc signaling pathway.

    Conclusions:

    • Circ-IP6K2 acts as a tumor suppressor in ccRCC by modulating the miR-1292-5p/CAMK2N1 axis and inhibiting the β-catenin/c-Myc pathway.
    • These findings highlight circ-IP6K2 as a potential therapeutic target for ccRCC treatment.
    • The study provides novel insights into the molecular mechanisms driving ccRCC progression.