Evidence map›Paper›PMID 36759819›Full record

ReviewCell communication and signaling : CCS2023

Targeting and regulation of autophagy in hepatocellular carcinoma: revisiting the molecular interactions and mechanisms for new therapy approaches.

Mehrdad Hashemi, Niloufar Nadafzadeh, Mohammad Hassan Imani, Romina Rajabi, Setayesh Ziaolhagh, Seyedeh Delaram Bayanzadeh, Raheleh Norouzi, Reihaneh Rafiei, Zeinab Khazaei Koohpar, Behnaz Raei and 7 more

Open access · goldAbstract readVideo-Audio MediaReview
In one paragraph

Review in Cell communication and signaling : CCS, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed, 1 pooled it
8.4field-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

29 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Pooled it
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  5. Review
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  20. Long Non-coding RNAs Influence Aging Process of Sciatic Nerves in SD Rats.Combinatorial chemistry & high throughput screening · 2024
    Article
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

17 authors at 8 institutions in 3 countries.

Mehrdad HashemiDepartment of Genetics, Faculty of Advanced Science and Technology, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.
Niloufar NadafzadehFaculty of Veterinary Medicine, Science and Research Branch, Islamic Azad University, Tehran, Iran.
Mohammad Hassan ImaniDepartment of Clinical Science, Faculty of Veterinary Medicine, Shahr-E Kord Branch, Islamic Azad University, Tehran, Chaharmahal and Bakhtiari, Iran.
Romina RajabiFaculty of Veterinary Medicine, Science and Research Branch, Islamic Azad University, Tehran, Iran.
Setayesh ZiaolhaghFaculty of Veterinary Medicine, Science and Research Branch, Islamic Azad University, Tehran, Iran.
Seyedeh Delaram BayanzadehFaculty of Veterinary Medicine, Science and Research Branch, Islamic Azad University, Tehran, Iran.
Raheleh NorouziFarhikhtegan Medical Convergence Sciences Research Center, Farhikhtegan Hospital Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.
Reihaneh RafieiFarhikhtegan Medical Convergence Sciences Research Center, Farhikhtegan Hospital Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.
Zeinab Khazaei KoohparDepartment of Cell and Molecular Biology, Faculty of Biological Sciences, Tonekabon Branch, Islamic Azad University, Tonekabon, Iran.
Behnaz RaeiFarhikhtegan Medical Convergence Sciences Research Center, Farhikhtegan Hospital Tehran Medical Sciences, Islamic Azad University, Tehran, Iran.
Mohammad Arad ZandiehDepartment of Food Hygiene and Quality Control, Division of Epidemiology, Faculty of Veterinary Medicine, University of Tehran, Tehran, Iran. m.aradzandieh@ut.ac.ir.
Shokooh SalimimoghadamDepartment of Biochemistry and Molecular Biology, Faculty of Veterinary Medicine, Shahid Chamran University of Ahvaz, Ahvaz, Iran.
Maliheh EntezariDepartment of Genetics, Faculty of Advanced Science and Technology, Tehran Medical Sciences, Islamic Azad University, Tehran, Iran. mentezari@iautmu.ac.ir.
Afshin TaheriazamFarhikhtegan Medical Convergence Sciences Research Center, Farhikhtegan Hospital Tehran Medical Sciences, Islamic Azad University, Tehran, Iran. a.taheriazam@iautmu.ac.ir.
Athanasios AlexiouDepartment of Science and Engineering, Novel Global Community Educational Foundation, Hebersham, Australia.
Marios PapadakisDepartment of Surgery II, University Hospital Witten-Herdecke, University of Witten-Herdecke, Heusnerstrasse 40, 42283, Wuppertal, Germany. marios_papadakis@yahoo.gr.
Shing Cheng TanUKM Medical Molecular Biology Institute, Universiti Kebangsaan Malaysia, Kuala Lumpur, Malaysia.
Islamic Azad University Medical Branch of Tehran · IRIslamic Azad University, Science and Research Branch · IRIslamic Azad University of Shahrekord · IRIslamic Azad University Tonekabon · IRShahid Chamran University of Ahvaz · IRUniversity Kebangsaan Malaysia Medical Centre · MYUniversity of Tehran · IRWitten/Herdecke University · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Autophagy is an evolutionarily conserved process that plays a role in regulating homeostasis under physiological conditions. However, dysregulation of autophagy is observed in the development of human diseases, especially cancer. Autophagy has reciprocal functions in cancer and may be responsible for either survival or death. Hepatocellular carcinoma (HCC) is one of the most lethal and common malignancies of the liver, and smoking, infection, and alcohol consumption can lead to its development. Genetic mutations and alterations in molecular processes can exacerbate the progression of HCC. The function of autophagy in HCC is controversial and may be both tumor suppressive and tumor promoting. Activation of autophagy may affect apoptosis in HCC and is a regulator of proliferation and glucose metabolism. Induction of autophagy may promote tumor metastasis via induction of EMT. In addition, autophagy is a regulator of stem cell formation in HCC, and pro-survival autophagy leads to cancer cell resistance to chemotherapy and radiotherapy. Targeting autophagy impairs growth and metastasis in HCC and improves tumor cell response to therapy. Of note, a large number of signaling pathways such as STAT3, Wnt, miRNAs, lncRNAs, and circRNAs regulate autophagy in HCC. Moreover, regulation of autophagy (induction or inhibition) by antitumor agents could be suggested for effective treatment of HCC. In this paper, we comprehensively review the role and mechanisms of autophagy in HCC and discuss the potential benefit of targeting this process in the treatment of the cancer. Video Abstract.

Indexed as

Carcinoma, HepatocellularLiver NeoplasmsAutophagyCell Line, TumorCell ProliferationGene Expression Regulation, NeoplasticHumansAutophagyChemoresistanceHepatocellular carcinomaMetastasisStemness

Identifiers

PMID36759819
PMCPMC9912665
OpenAlexW4319737147

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.