Evidence map›Paper›PMID 39428480›Full record

ArticleCancer cell international2024

Curcumin attenuates smoking and drinking activated NF-κB/IL-6 inflammatory signaling axis in cervical cancer.

Vivek K Kashyap, Prashanth K B Nagesh, Ajay K Singh, Andrew Massey, Godwin P Darkwah, Aaron George, Sheema Khan, Bilal B Hafeez, Nadeem Zafar, Santosh Kumar and 4 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cancer cell international, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
7citing papers in PubMed, 1 pooled it
–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

7 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Review
  3. Review
  4. Review
  5. Article
  6. Review
  7. 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

14 authors.

Vivek K KashyapDivision of Cancer Immunology and Microbiology, Medicine and Oncology Integrated Service Unit, School of Medicine, University of Texas Rio Grande Valley, McAllen, TX, 78504, USA.
Prashanth K B NageshDivision of Cancer Immunology and Microbiology, Medicine and Oncology Integrated Service Unit, School of Medicine, University of Texas Rio Grande Valley, McAllen, TX, 78504, USA.
Ajay K SinghDepartment of Pharmaceutical Sciences, University of Tennessee Health Science Center, Memphis, TN, 38163, USA.
Andrew MasseyDivision of Cancer Immunology and Microbiology, Medicine and Oncology Integrated Service Unit, School of Medicine, University of Texas Rio Grande Valley, McAllen, TX, 78504, USA.
Godwin P DarkwahDivision of Cancer Immunology and Microbiology, Medicine and Oncology Integrated Service Unit, School of Medicine, University of Texas Rio Grande Valley, McAllen, TX, 78504, USA.
Aaron GeorgeSouth Texas Center of Excellence in Cancer Research (ST-CECR), McAllen, TX, 78504, USA.
Sheema KhanDivision of Cancer Immunology and Microbiology, Medicine and Oncology Integrated Service Unit, School of Medicine, University of Texas Rio Grande Valley, McAllen, TX, 78504, USA.
Bilal B HafeezDivision of Cancer Immunology and Microbiology, Medicine and Oncology Integrated Service Unit, School of Medicine, University of Texas Rio Grande Valley, McAllen, TX, 78504, USA.
Nadeem ZafarDepartment of Pathology, University of Washington, Seattle, DC, 98195, USA.
Santosh KumarDepartment of Pharmaceutical Sciences, University of Tennessee Health Science Center, Memphis, TN, 38163, USA.
Namita SinhaDepartment of Pharmaceutical Sciences, University of Tennessee Health Science Center, Memphis, TN, 38163, USA.
Murali M YallapuDivision of Cancer Immunology and Microbiology, Medicine and Oncology Integrated Service Unit, School of Medicine, University of Texas Rio Grande Valley, McAllen, TX, 78504, USA.
Meena JaggiDivision of Cancer Immunology and Microbiology, Medicine and Oncology Integrated Service Unit, School of Medicine, University of Texas Rio Grande Valley, McAllen, TX, 78504, USA.
Subhash C ChauhanDivision of Cancer Immunology and Microbiology, Medicine and Oncology Integrated Service Unit, School of Medicine, University of Texas Rio Grande Valley, McAllen, TX, 78504, USA. subhash.chauhan@utrgv.edu.

Funding

X-RAY CRYSTALLOGRAPHYP30CA008748 · NCI · SLOAN-KETTERING INSTITUTE FOR CANCER RES · PI SELWYN M VICKERS · 1985 to 2026
$347.4M
Etiology of cervical cancer health disparity in American Indian womenU01CA162106 · NCI · UNIVERSITY OF TENNESSEE HEALTH SCI CTR · PI CHAUHAN, SUBHASH C., JAGGI, MEENA · 2012 to 2016
$1.5M
NCI NIH HHS P30 CA008748NCI NIH HHS U01 CA162106NIH HHS U01CA162106
6 · The paper itself

Abstract

backgroundHigh-risk strains of HPV are known to cause cervical cancer. Multiple clinical studies have emphasized that smoking and drinking are critical risk factors for cervical cancer and its high-grade precursors. In this study, we investigated if smoking and/or drinking augment the molecular mechanisms of cervical carcinogenesis and defined a potential therapeutic approach for their attenuation.

methodsThe impact of benzo[a]pyrene (B[a]P) and/or ethanol (EtOH) exposure on cervical cancer cells was assessed by measuring changes in their cell migration and invasion characteristics. Expression of HPV16 E6/E7, NF-κB, cytokines, and inflammation mediators was determined using qRT-PCR, immunoblotting, ELISA, luciferase reporter assay, and confocal microscopy. Herein, we used curcumin (Cur), and PLGA nanoparticle formulation of curcumin (PLGA-Cur) and determined effectiveness of free Cur and PLGA-Cur formulation on smoking and drinking activated NF-κB/IL-6 mediated inflammatory signaling pathways using in vitro cervical cancer models.

resultsTreatments with B[a]P and/or EtOH altered the expression of HPV16 E6/E7 oncogenes and EMT markers in cervical cancer cells; it also enhanced migration and invasion. In addition, B[a]P and/or EtOH exposure promoted inflammation pathways through TNF-α and NF-κB signaling, leading to IL-6 upregulation and activation of VEGF. The molecular effects caused by B[a]P and/or EtOH exposure were effectively attenuated by curcumin (Cur)/PLGA-Cur treatment.

conclusionsThese data suggest a molecular link between smoking, drinking, and HPV infectivity in cervical carcinogenesis. In addition, attenuation of these effects by treatment with Cur/PLGA-Cur treatment, implies the role of curcumin in cervical cancer prevention and treatment.

Indexed as

Benzo[a]pyreneCervical cancerCigarette smoking and drinkingCur/PLGA-CurHPV16 E6/E7NanoformulationNF-κB

Identifiers

PMID39428480
PMCPMC11492755

What OpenQuestion holds

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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.