Evidence map›Paper›PMID 33628386›Full record

ReviewOxidative medicine and cellular longevity2021

Autophagy Paradox of Cancer: Role, Regulation, and Duality.

Amit Kumar Verma, Prahalad Singh Bharti, Sahar Rafat, Deepti Bhatt, Yamini Goyal, Kamlesh Kumar Pandey, Sanjeev Ranjan, Saleh A Almatroodi, Mohammed A Alsahli, Arshad Husain Rahmani and 2 more

Open access · hybridAbstract readReview
In one paragraph

Review in Oxidative medicine and cellular longevity, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
7.8field-weighted citation impact, top 2% of its field
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

49 citing papers in PubMed, 73 citations in OpenAlex.

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  14. Dual role of autophagy in bone metastasis: mechanistic insights and therapeutic targeting.American journal of clinical and experimental urology · 2025
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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

12 authors at 3 institutions in 2 countries.

Amit Kumar VermaDepartment of Biotechnology, Jamia Millia Islamia, New Delhi, India.
Prahalad Singh BhartiDepartment of Biophysics, All India Institutes of Medical Sciences, New Delhi, India.
Sahar RafatDepartment of Biotechnology, Jamia Millia Islamia, New Delhi, India.
Deepti BhattDepartment of Biotechnology, Jamia Millia Islamia, New Delhi, India.
Yamini GoyalDepartment of Biotechnology, Jamia Millia Islamia, New Delhi, India.
Kamlesh Kumar PandeyDepartment of Anatomy, All India Institutes of Medical Sciences, New Delhi, India.
Sanjeev RanjanInstitute of Biomedicine, Cell and Tissue Imaging Unit, Finland.
Saleh A AlmatroodiDepartment of Medical Laboratories, College of Applied Medical Science, Qassim University, Buraidah, Saudi Arabia.
Mohammed A AlsahliDepartment of Medical Laboratories, College of Applied Medical Science, Qassim University, Buraidah, Saudi Arabia.
Arshad Husain RahmaniDepartment of Medical Laboratories, College of Applied Medical Science, Qassim University, Buraidah, Saudi Arabia.ORCID https://orcid.org/0000-0002-1329-1391
Ahmad AlmatroudiDepartment of Medical Laboratories, College of Applied Medical Science, Qassim University, Buraidah, Saudi Arabia.ORCID https://orcid.org/0000-0002-1491-6402
Kapil DevDepartment of Biotechnology, Jamia Millia Islamia, New Delhi, India.ORCID https://orcid.org/0000-0002-3995-2370
Department of Biotechnology · INQassim University · SAAll India Institute of Medical Sciences · IN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy, a catabolic process, degrades damaged and defective cellular materials through lysosomes, thus working as a recycling mechanism of the cell. It is an evolutionarily conserved and highly regulated process that plays an important role in maintaining cellular homeostasis. Autophagy is constitutively active at the basal level; however, it gets enhanced to meet cellular needs in various stress conditions. The process involves various autophagy-related genes that ultimately lead to the degradation of targeted cytosolic substrates. Many factors modulate both upstream and downstream autophagy pathways like nutritional status, energy level, growth factors, hypoxic conditions, and localization of p53. Any problem in executing autophagy can lead to various pathological conditions including neurodegeneration, aging, and cancer. In cancer, autophagy plays a contradictory role; it inhibits the formation of tumors, whereas, during advanced stages, autophagy promotes tumor progression. Besides, autophagy protects the tumor from various therapies by providing recycled nutrition and energy to the tumor cells. Autophagy is stimulated by tumor suppressor proteins, whereas it gets inhibited by oncogenes. Due to its dynamic and dual role in the pathogenesis of cancer, autophagy provides promising opportunities in developing novel and effective cancer therapies along with managing chemoresistant cancers. In this article, we summarize different strategies that can modulate autophagy in cancer to overcome the major obstacle, i.e., resistance developed in cancer to anticancer therapies.

Indexed as

AutophagyAnimalsDrug Resistance, NeoplasmHumansImmune SystemModels, BiologicalNeoplasmsSignal Transduction

Identifiers

PMID33628386
PMCPMC7892237
OpenAlexW3128011759

What OpenQuestion holds

Textmetadata
LicenceCC BY
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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.