Evidence map›Paper›PMID 35317831›Full record

ReviewJournal of experimental & clinical cancer research : CR2022

Targeting autophagy in prostate cancer: preclinical and clinical evidence for therapeutic response.

Milad Ashrafizadeh, Mahshid Deldar Abad Paskeh, Sepideh Mirzaei, Mohammad Hossein Gholami, Ali Zarrabi, Farid Hashemi, Kiavash Hushmandi, Mehrdad Hashemi, Noushin Nabavi, Francesco Crea and 4 more

Open access · goldAbstract readReview
In one paragraph

Review in Journal of experimental & clinical cancer research : CR, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 1 pooled it
20.7field-weighted citation impact, top 1% 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

71 citing papers in PubMed, 1 synthesis or guideline pooled it, 138 citations in OpenAlex.

  1. Pooled it
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  16. Autophagy: The convergence point of aging and cancer.Biochemistry and biophysics reports · 2025
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11 more citing papers are in PubMed but not listed here.

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

14 authors at 11 institutions in 7 countries.

Milad AshrafizadehFaculty of Engineering and Natural Sciences, Sabanci University, Orta Mahalle, Üniversite Caddesi No. 27, Orhanlı, Tuzla, 34956, Istanbul, Turkey. milad.ashrafizadeh@sabanciuniv.edu.
Mahshid Deldar Abad PaskehDepartment of Genetics, Faculty of Advanced Science and Technology, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.
Sepideh MirzaeiDepartment of Biology, Faculty of Science, Islamic Azad University, Science and Research Branch, Tehran, Iran.
Mohammad Hossein GholamiFaculty of Veterinary Medicine, Kazerun Branch, Islamic Azad University, Kazerun, Iran.
Ali ZarrabiDepartment of Biomedical Engineering, Faculty of Engineering and Natural Sciences, Istinye University, 34396, Istanbul, Turkey.ORCID http://orcid.org/0000-0003-0391-1769
Farid HashemiDepartment of Comparative Biosciences, Faculty of Veterinary Medicine, University of Tehran, Tehran, 1417466191, Iran.
Kiavash HushmandiDepartment of Food Hygiene and Quality Control, Division of Epidemiology & Zoonoses, Faculty of Veterinary Medicine University of Tehran, Tehran, Iran.
Mehrdad HashemiDepartment of Genetics, Faculty of Advanced Science and Technology, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.
Noushin NabaviDepartment of Urological Sciences and Vancouver Prostate Centre, University of British Columbia, V6H3Z6, Vancouver, BC, Canada.
Francesco CreaCancer Research Group-School of Life Health and Chemical Sciences, The Open University, Walton Hall, Milton Keynes, MK7 6AA, UK.
Jun RenDepartment of Laboratory Medicine and Pathology, University of Washington, Seattle, WA, 98195, USA.ORCID http://orcid.org/0000-0002-0275-0783
Daniel J KlionskyLife Sciences Institute & Department of Molecular, Cellular and Developmental Biology, University of Michigan, Ann Arbor, MI, 48109, USA.ORCID http://orcid.org/0000-0002-7828-8118
Alan Prem KumarCancer Science Institute of Singapore and Department of Pharmacology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore, 117599, Singapore. apkumar@nus.edu.sg.ORCID http://orcid.org/0000-0002-3754-5712
Yuzhuo WangDepartment of Urological Sciences and Vancouver Prostate Centre, University of British Columbia, V6H3Z6, Vancouver, BC, Canada. ywang@bccrc.ca.ORCID http://orcid.org/0000-0002-9749-8591
Islamic Azad University Medical Branch of Tehran · IRUniversity of British Columbia · CAUniversity of Tehran · IRIslamic Azad University Kazeron · IRIslamic Azad University, Science and Research Branch · IRIstinye University · TRNational University of Singapore · SGSabancı Üniversitesi · TRThe Open University · GBUniversity of Michigan · USUniversity of Washington · US

Funding

CIHR 141635Ministry of Education - Singapore MOE-T2EP30120-0016Terry Fox Foundation 1062
6 · The paper itself

Abstract

Prostate cancer is a leading cause of death worldwide and new estimates revealed prostate cancer as the leading cause of death in men in 2021. Therefore, new strategies are pertinent in the treatment of this malignant disease. Macroautophagy/autophagy is a "self-degradation" mechanism capable of facilitating the turnover of long-lived and toxic macromolecules and organelles. Recently, attention has been drawn towards the role of autophagy in cancer and how its modulation provides effective cancer therapy. In the present review, we provide a mechanistic discussion of autophagy in prostate cancer. Autophagy can promote/inhibit proliferation and survival of prostate cancer cells. Besides, metastasis of prostate cancer cells is affected (via induction and inhibition) by autophagy. Autophagy can affect the response of prostate cancer cells to therapy such as chemotherapy and radiotherapy, given the close association between autophagy and apoptosis. Increasing evidence has demonstrated that upstream mediators such as AMPK, non-coding RNAs, KLF5, MTOR and others regulate autophagy in prostate cancer. Anti-tumor compounds, for instance phytochemicals, dually inhibit or induce autophagy in prostate cancer therapy. For improving prostate cancer therapy, nanotherapeutics such as chitosan nanoparticles have been developed. With respect to the context-dependent role of autophagy in prostate cancer, genetic tools such as siRNA and CRISPR-Cas9 can be utilized for targeting autophagic genes. Finally, these findings can be translated into preclinical and clinical studies to improve survival and prognosis of prostate cancer patients.

Indexed as

AutophagyHumansMaleProstatic NeoplasmsAnti-tumor compoundsAutophagyBiomarkerNon-coding RNAsProstate cancerTherapy response

Identifiers

PMID35317831
PMCPMC8939209
OpenAlexW4220784485

What Socratic holds

Textmetadata
LicenceCC BY
Read underepoch 390

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 Socratic graph.