Long noncoding RNA SNHG12 promotes tumour progression and sunitinib resistance by upregulating CDCA3 in renal cell

Related Experiment Video

Updated: Dec 15, 2025

Repression of Multiple Myeloma Cell Growth In Vivo by Single-wall Carbon Nanotube SWCNT-delivered MALAT1 Antisense Oligos
07:24

Repression of Multiple Myeloma Cell Growth In Vivo by Single-wall Carbon Nanotube SWCNT-delivered MALAT1 Antisense Oligos

Published on: December 13, 2018

6.7K

Yuenan Liu1, Gong Cheng1, Ziwei Huang2

  • 1Department of Urology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, No. 1277 Jiefang Avenue, 430022, Wuhan, China.

Cell Death & Disease
|July 10, 2020
PubMed

Insights

Long noncoding RNA SNHG12 promotes renal cell carcinoma (RCC) progression and resistance to sunitinib treatment. Targeting the SNHG12/SP1/CDCA3 pathway may overcome drug resistance in RCC patients.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Renal cell carcinoma (RCC) is a common urinary system malignancy.
  • Acquired resistance to targeted therapies, like sunitinib, is a significant clinical challenge in RCC.
  • The role of long noncoding RNA SNHG12 (lncRNA SNHG12) in RCC drug resistance is not well understood.

Purpose of the Study:

  • To investigate the function of lncRNA SNHG12 in the development of sunitinib resistance in renal cell carcinoma.
  • To elucidate the molecular mechanism underlying SNHG12's role in RCC progression and drug resistance.

Main Methods:

  • Analysis of SNHG12 expression in RCC tissues and cell lines.
  • In vitro studies assessing the impact of SNHG12 on RCC cell proliferation, migration, and invasion.
  • Investigation of the SNHG12/SP1/CDCA3 interaction and its effect on CDCA3 expression.
  • In vivo tumor xenograft models to evaluate SNHG12's role in tumor growth and sunitinib resistance.

Main Results:

  • SNHG12 was significantly upregulated in RCC tissues and sunitinib-resistant cells, correlating with poor prognosis.
  • Overexpression of SNHG12 enhanced RCC cell proliferation, migration, invasion, and sunitinib resistance.
  • SNHG12 stabilized SP1 by inhibiting its ubiquitylation-dependent proteolysis, leading to increased CDCA3 expression.
  • Knockdown of SNHG12 reversed sunitinib resistance and reduced tumor growth in vivo.

Conclusions:

  • The lncRNA SNHG12/SP1/CDCA3 axis drives RCC progression and promotes resistance to sunitinib.
  • Targeting the SNHG12/SP1/CDCA3 pathway represents a potential therapeutic strategy for overcoming sunitinib resistance in RCC.

Related Concept Videos

lncRNA - Long Non-coding RNAs02:39

lncRNA - Long Non-coding RNAs

In humans, more than 80% of the genome gets transcribed. However, only around 2% of the genome codes for proteins. The remaining part produces non-coding RNAs which includes ribosomal RNAs, transfer RNAs, telomerase RNAs, and regulatory RNAs, among other types. A large number of regulatory non-coding RNAs have been classified into two groups depending upon their length – small non-coding RNAs, such as microRNA, which are less than 200 nucleotides in length, and long non-coding RNA...
9.6K
lncRNA - Long Non-coding RNAs02:39

lncRNA - Long Non-coding RNAs

3.3K
mTOR Signaling and Cancer Progression03:03

mTOR Signaling and Cancer Progression

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...
4.5K
Abnormal Proliferation02:23

Abnormal Proliferation

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...
5.0K
Inhibition of Cdk Activity02:34

Inhibition of Cdk Activity

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...
5.4K
The Retinoblastoma Gene01:20

The Retinoblastoma Gene

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,...
4.6K