Related Experiment Video

Updated: Aug 9, 2025

Dual CRISPR-Interference Strategy for Targeting Synthetic Lethal Interactions Between Non-Coding RNAs in Cancer Cells
07:23

Dual CRISPR-Interference Strategy for Targeting Synthetic Lethal Interactions Between Non-Coding RNAs in Cancer Cells

Published on: May 30, 2025

511

Functional Relevance of the Long Intergenic Non-Coding RNA Regulator of Reprogramming (Linc-ROR) in Cancer

José A Peña-Flores1, Diego Enríquez-Espinoza1, Daniela Muela-Campos1

  • 1Faculty of Dentistry, Universidad Autónoma de Chihuahua, Chihuahua 31000, Mexico.

Non-Coding RNA
|February 24, 2023
PubMed

Insights

The long intergenic non-coding RNA regulator of reprogramming (linc-ROR) is a key player in cancer. This review details its role in tumor growth, spread, and drug resistance, aiding targeted therapies.

Area of Science:

  • Oncology
  • Molecular Biology
  • Genetics

Background:

  • Cancer causes over 10 million deaths annually, with metastasis and drug resistance posing significant therapeutic challenges.
  • Long non-coding RNAs (lncRNAs) are increasingly recognized as crucial in cancer development.
  • The long intergenic non-coding RNA regulator of reprogramming (linc-ROR) is frequently dysregulated in various cancers.

Purpose of the Study:

  • To provide an updated and comprehensive understanding of linc-ROR's multifaceted roles in cancer.
  • To elucidate the molecular mechanisms underlying linc-ROR's involvement in tumorigenesis, progression, metastasis, and chemoresistance.
  • To highlight the potential of linc-ROR as a diagnostic and prognostic biomarker and therapeutic target.

Main Methods:

  • Literature review of recent studies on linc-ROR in cancer.
  • Analysis of molecular mechanisms, including linc-ROR's function as a competing endogenous RNA (ceRNA).
  • Synthesis of evidence regarding linc-ROR's implications across different cancer stages and therapeutic contexts.

Main Results:

  • linc-ROR acts as an onco-lncRNA, sequestering microRNAs and promoting cancer progression.
  • Dysregulation of linc-ROR is linked to key hallmarks of cancer, including proliferation, migration, invasion, and drug resistance.
  • Emerging evidence points to linc-ROR's involvement in epithelial-mesenchymal transition and cancer stem cell maintenance.

Conclusions:

  • linc-ROR is a critical oncogenic lncRNA with significant implications in cancer initiation, progression, metastasis, and chemoresistance.
  • Targeting linc-ROR offers a promising avenue for developing novel diagnostic, prognostic, and therapeutic strategies in precision oncology.
  • Further research into linc-ROR's intricate molecular pathways is essential for advancing cancer treatment.
Keywords:
cancer invasioncancer metastasiscancer progressioncancer proliferationdrug resistancelinc-RORlincRNA-RORlncRNA

More Related Videos

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis11:44

Analysis of Combinatorial miRNA Treatments to Regulate Cell Cycle and Angiogenesis

Published on: March 30, 2019

7.7K
CAM-Delam Assay to Score Metastatic Properties by Quantifying Delamination and Invasion Capacity of Cancer Cells12:14

CAM-Delam Assay to Score Metastatic Properties by Quantifying Delamination and Invasion Capacity of Cancer Cells

Published on: June 2, 2022

2.7K

Related Concept Videos

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...
3.8K
Metastasis02:30

Metastasis

Metastasis is the spread of cancer cells from the original site to distant locations in the body. Cancer cells can spread via blood vessels (hematogenous) as well as lymph vessels in the body.
Epithelial-to-Mesenchymal Transition
The epithelial-to-mesenchymal transition or EMT is a developmental process commonly observed in wound healing, embryogenesis, and cancer metastasis. EMT is induced by transforming growth factor-beta (TGF-β) or receptor tyrosine kinase (RTK) ligands, which further...
5.6K
Adaptive Mechanisms in Cancer Cells02:53

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...
5.9K
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...
8.7K
Treatment Resistant Cancers02:56

Treatment Resistant Cancers

Cancer is the second leading cause of death in the United States. A cancer cell is genetically unstable and hence can mutate faster. They can also modify their microenvironment and escape immune surveillance. The difficulties in treating cancer are further compounded by the emergence of rapid resistance to anticancer drugs. The most common ways to attain resistance in cancer cells include alteration in drug transport and metabolism, modification of drug target, elevated DNA damage response, or...
3.4K
PI3K/mTOR/AKT Signaling Pathway01:22

PI3K/mTOR/AKT Signaling Pathway

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...
3.8K