Evidence map›Paper›PMID 26621832›Full record

ArticleOncotarget2015

Proteasome inhibition mediates p53 reactivation and anti-cancer activity of 6-gingerol in cervical cancer cells.

Namrata Rastogi, Shivali Duggal, Shailendra Kumar Singh, Konica Porwal, Vikas Kumar Srivastava, Rakesh Maurya, M L B Bhatt, Durga Prasad Mishra

Open access · diamondAbstract read
In one paragraph

Article in Oncotarget, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
31citing papers in PubMed, 2 pooled it
5.2field-weighted citation impact, top 5% 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

31 citing papers in PubMed, 2 syntheses or guidelines pooled it, 107 citations in OpenAlex.

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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

8 authors at 3 institutions in 2 countries.

Namrata RastogiCell Death Research Laboratory, Division of Endocrinology, CSIR-Central Drug Research Institute, Lucknow, India.
Shivali DuggalDepartment of Radiotherapy, King George Medical University, Lucknow, India.
Shailendra Kumar SinghDepartment of Host Defense, WPI Immunology Frontier Research Center, Osaka University, Suita, Osaka, Japan.
Konica PorwalCell Death Research Laboratory, Division of Endocrinology, CSIR-Central Drug Research Institute, Lucknow, India.
Vikas Kumar SrivastavaDepartment of Radiotherapy, King George Medical University, Lucknow, India.
Rakesh MauryaMedicinal Process Chemistry Division, CSIR-Central Drug Research Institute, Lucknow, India.
M L B BhattDepartment of Radiotherapy, King George Medical University, Lucknow, India.
Durga Prasad MishraCell Death Research Laboratory, Division of Endocrinology, CSIR-Central Drug Research Institute, Lucknow, India.
Central Drug Research Institute · INKing George's Medical University · INOsaka University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Human papilloma virus (HPV) expressing E6 and E7 oncoproteins, is known to inactivate the tumor suppressor p53 through proteasomal degradation in cervical cancers. Therefore, use of small molecules for inhibition of proteasome function and induction of p53 reactivation is a promising strategy for induction of apoptosis in cervical cancer cells. The polyphenolic alkanone, 6-Gingerol (6G), present in the pungent extracts of ginger (Zingiber officinale Roscoe) has shown potent anti-tumorigenic and pro-apoptotic activities against a variety of cancers. In this study we explored the molecular mechanism of action of 6G in human cervical cancer cells in vitro and in vivo. 6G potently inhibited proliferation of the HPV positive cervical cancer cells. 6G was found to: (i) inhibit the chymotrypsin activity of proteasomes, (ii) induce reactivation of p53, (iii) increase levels of p21, (iv) induce DNA damage and G2/M cell cycle arrest, (v) alter expression levels of p53-associated apoptotic markers like, cleaved caspase-3 and PARP, and (vi) potentiate the cytotoxicity of cisplatin. 6G treatment induced significant reduction of tumor volume, tumor weight, proteasome inhibition and p53 accumulation in HeLa xenograft tumor cells in vivo. The 6G treatment was devoid of toxic effects as it did not affect body weights, hematological and osteogenic parameters. Taken together, our data underscores the therapeutic and chemosensitizing effects of 6G in the management and treatment of cervical cancer.

Indexed as

AnimalsAntineoplastic AgentsBlotting, WesternCatecholsCell ProliferationFatty AlcoholsFemaleFlow CytometryHeLa CellsHumansMaleMiceMice, NudeMicroscopy, ConfocalMolecular Docking SimulationPapillomavirus InfectionsAntineoplastic AgentsCatecholsFatty AlcoholsgingerolProteasome Endopeptidase ComplexRNA, Small InterferingTumor Suppressor Protein p536-gingerolcervical cancerChromosome SectionHPVp53 reactivationproteasome

Identifiers

PMID26621832
PMCPMC4791234
OpenAlexW2180047526

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Registered trials

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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.