Evidence map›Paper›PMID 40898219›Full record

ReviewCancer cell international2025

Crosstalk between noncoding RNAs and autophagy in renal cell carcinoma: Deciphering molecular pathways and therapeutic prospects.

Mina Alimohammadi, Mojgan Noroozi, Alireza Mafi, Fateme Zare Khormizi, Amirhosein Abbasi, Najma Farahani, Seyedeh Mahdieh Khoshnazar, Mehrdad Hashemi, Afshin Taheriazam, Kiavash Hushmandi

Abstract readReview
In one paragraph

Review in Cancer cell international, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

10 authors.

Mina AlimohammadiDepartment of Immunology, School of Medicine, Shahid Beheshti University of Medical Sciences, Tehran, Iran.
Mojgan NorooziMolecular Medicine Research Center, Research Institute of Basic Medical Sciences, Rafsanjan University of Medical Sciences, Rafsanjan, Iran.
Alireza MafiNutrition and Food Security Research Center, Isfahan University of Medical Sciences, Isfahan, Iran.
Fateme Zare KhormiziDepartment of Biology, Yazd University, Yazd, Iran.
Amirhosein AbbasiDepartment of Cell and Molecular Sciences, Faculty of Biological Sciences, Kharazmi University, Tehran, Iran.
Najma FarahaniFarhikhtegan Medical Convergence Sciences Research Center, Farhikhtegan Hospital, TMs.C., Islamic Azad University, Tehran, Iran.
Seyedeh Mahdieh KhoshnazarPhysiology Research Center, Institute of Neuropharmacology, Kerman University of Medical Sciences, Kerman, Iran. m_khoshnazar@kmu.ac.ir.
Mehrdad HashemiFarhikhtegan Medical Convergence Sciences Research Center, Farhikhtegan Hospital, TMs.C., Islamic Azad University, Tehran, Iran. mhashemi@iautmu.ac.ir.
Afshin TaheriazamFarhikhtegan Medical Convergence Sciences Research Center, Farhikhtegan Hospital, TMs.C., Islamic Azad University, Tehran, Iran. a.taheriazam@iautmu.ac.ir.
Kiavash HushmandiNephrology and Urology Research Center, Clinical Sciences Institute, Baqiyatallah University of Medical Sciences, Tehran, Iran. houshmandi.kia7@ut.ac.ir.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

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.

Indexed as

Autophagy regulationNon-coding RNAs (ncRNAs)Renal cell carcinoma (RCC)Signaling pathwaysTherapeutic targetsTreatment resistance

Identifiers

PMID40898219
PMCPMC12403932

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.