Evidence map›Paper›PMID 35941592›Full record

ReviewCancer cell international2022

Targeting Ras-ERK cascade by bioactive natural products for potential treatment of cancer: an updated overview.

Eunus S Ali, Shamima Akter, Sarker Ramproshad, Banani Mondal, Thoufiqul Alam Riaz, Muhammad Torequl Islam, Ishaq N Khan, Anca Oana Docea, Daniela Calina, Javad Sharifi-Rad and 1 more

Open access · goldAbstract readReview
In one paragraph

Review in Cancer cell international, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
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, 49 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

11 authors at 8 institutions in 8 countries.

Eunus S AliCollege of Medicine and Public Health, Flinders University, Bedford Park, 5042, Australia.
Shamima AkterDepartment of Bioinformatics and Computational Biology, George Mason University, Fairfax, VA, 22030, USA.
Sarker RamproshadDepartment of Pharmacy, Ranada Prasad Shaha University, Narayanganj, 1400, Bangladesh.
Banani MondalDepartment of Pharmacy, Ranada Prasad Shaha University, Narayanganj, 1400, Bangladesh.
Thoufiqul Alam RiazDepartment of Pharmacology and Institute of New Drug Development, Jeonbuk National University Medical School, Jeonju, 54907, Republic of Korea.
Muhammad Torequl IslamDepartment of Pharmacy, Life Science Faculty, Bangabandhu Sheikh Mujibur Rahman Science and Technology University, Gopalganj, 8100, Bangladesh.
Ishaq N KhanInstitute of Basic Medical Sciences, Khyber Medical University, Peshawar, 25100, Pakistan.
Anca Oana DoceaDepartment of Toxicology, University of Medicine and Pharmacy of Craiova, 200349, Craiova, Romania.
Daniela CalinaDepartment of Clinical Pharmacy, University of Medicine and Pharmacy of Craiova, 200349, Craiova, Romania. calinadaniela@gmail.com.
Javad Sharifi-RadFacultad de Medicina, Universidad del Azuay, Cuenca, Ecuador. javad.sharifirad@gmail.com.
William C ChoDepartment of Clinical Oncology, Queen Elizabeth Hospital, Kowloon, Hong Kong. chocs@ha.org.hk.
University of Medicine and Pharmacy of Craiova · ROBangabandhu Sheikh Mujibur Rahman Science and Technology University · BDFlinders University · AUGeorge Mason University · USHospital Authority · CNJeonbuk National University · KRKhyber Medical University · PKUniversidad del Azuay · EC

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

MAPK (mitogen-activated protein kinase) or ERK (extracellular-signal-regulated kinase) pathway is an important link in the transition from extracellular signals to intracellular responses. Because of genetic and epigenetic changes, signaling cascades are altered in a variety of diseases, including cancer. Extant studies on the homeostatic and pathologic behavior of MAPK signaling have been conducted; however, much remains to be explored in preclinical and clinical research in terms of regulation and action models. MAPK has implications for cancer therapy response, more specifically in response to experimental MAPK suppression, compensatory mechanisms are activated. The current study investigates MAPK as a very complex cell signaling pathway that plays roles in cancer treatment response, cellular normal conduit maintenance, and compensatory pathway activation. Most MAPK inhibitors, unfortunately, cause resistance by activating compensatory feedback loops in tumor cells and tumor microenvironment components. As a result, innovative combinatorial treatments for cancer management must be applied to limit the likelihood of alternate pathway initiation as a possibility for generating novel therapeutics based on incorporation in translational research. We summarize current knowledge about the implications of ERK (MAPK) in cancer, as well as bioactive products from plants, microbial organisms or marine organisms, as well as the correlation with their chemical structures, which modulate this pathway for the treatment of different types of cancer.

Indexed as

CancerChemopreventionChemoresistanceMAPK (ERK)Molecular mechanismsNatural bioactive compoundsRas oncogenesRas signaling

Identifiers

PMID35941592
PMCPMC9358858
OpenAlexW4290631486

What OpenQuestion 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 OpenQuestion graph.