Crosstalk between noncoding RNAs and autophagy in renal cell carcinoma: Deciphering molecular pathways and
Mina Alimohammadi1, Mojgan Noroozi2, Alireza Mafi3,4
1Department of Immunology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Abstract:
Renal cell carcinoma (RCC) is one of the most common and aggressive forms of kidney cancer, accounting for over 90% of cases. Despite advances in diagnosis and treatment, RCC is often detected at advanced stages and demonstrates poor response to traditional therapies such as chemotherapy, radiotherapy, and hormonal treatment. Consequently, novel molecular targets are urgently needed. Autophagy, a tightly regulated catabolic mechanism that preserves cellular homeostasis via degradation of damaged organelles and proteins, plays a dual role in RCC-acting both as a tumor suppressor in early stages and a tumor promoter under stress conditions. Recent studies have revealed that non-coding RNAs (ncRNAs), particularly long ncRNAs and microRNAs (miRNAs), are key regulators of autophagy in various cancers, including RCC. These ncRNAs influence the expression of autophagy-related genes and modulate critical signaling pathways such as PI3K/AKT/mTOR, AMPK, p53, and KEAP1/NRF2. By acting as molecular sponges, scaffolds, and transcriptional regulators, ncRNAs either enhance or suppress autophagic activity, thereby affecting tumor progression, metastasis, and treatment resistance. This review synthesizes current knowledge on the crosstalk between ncRNAs and autophagy in RCC. We identify specific ncRNAs involved in RCC pathogenesis, describe their regulatory mechanisms, and evaluate their potential as diagnostic biomarkers and therapeutic targets. Understanding these complex molecular interactions may lead to more effective, personalized treatment strategies and improved clinical outcomes for RCC patients.
Insights
Non-coding RNAs (ncRNAs) regulate autophagy, a cellular process with a dual role in kidney cancer. Understanding this interplay may reveal new diagnostic biomarkers and therapeutic targets for renal cell carcinoma (RCC).
Area of Science:
- Oncology
- Molecular Biology
- Biochemistry
Background:
- Renal cell carcinoma (RCC) is an aggressive kidney cancer often diagnosed at advanced stages.
- Traditional therapies show limited efficacy, necessitating novel molecular targets.
- Autophagy, a cellular degradation process, plays a complex role in RCC, acting as both a tumor suppressor and promoter.
Purpose of the Study:
- To review the current understanding of the interaction between non-coding RNAs (ncRNAs) and autophagy in renal cell carcinoma (RCC).
- To identify specific ncRNAs involved in RCC pathogenesis and their regulatory mechanisms.
- To evaluate the potential of ncRNAs and autophagy as diagnostic biomarkers and therapeutic targets for RCC.
Main Methods:
- Literature review synthesizing current knowledge on ncRNAs, autophagy, and RCC.
- Analysis of ncRNA regulatory mechanisms, including roles as molecular sponges, scaffolds, and transcriptional regulators.
- Examination of signaling pathways modulated by ncRNAs in autophagy, such as PI3K/AKT/mTOR, AMPK, p53, and KEAP1/NRF2.
Main Results:
- ncRNAs, including long ncRNAs and microRNAs (miRNAs), are key regulators of autophagy in RCC.
- These ncRNAs influence autophagy-related gene expression and modulate critical signaling pathways.
- ncRNAs can enhance or suppress autophagic activity, impacting tumor progression, metastasis, and treatment resistance.
Conclusions:
- The crosstalk between ncRNAs and autophagy is crucial in RCC pathogenesis.
- Specific ncRNAs hold potential as diagnostic biomarkers for early detection and prognosis.
- Targeting ncRNA-autophagy interactions may offer novel therapeutic strategies for personalized RCC treatment.
- Further research into these molecular interactions can improve clinical outcomes for RCC patients.
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