Evidence map›Paper›PMID 41619095›Full record

ReviewDiscover oncology2026

Ubiquitination and deubiquitination as critical modulators of NSCLC tumorigenesis and drug resistance.

Prasanna Srinivasan Ramalingam, Mohammad Afzal, Manjunath Mirle Rekha, Samir Sahoo, Surya Nath Pandey, Chandana Maji, Kavita Goyal, Haider Ali, Sachin Kumar Singh, Gaurav Gupta and 3 more

Abstract readReview
In one paragraph

Review in Discover oncology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

13 authors.

Prasanna Srinivasan RamalingamProtein Engineering Lab, School of Biosciences and Technology, Vellore Institute of Technology, Katpadi, Vellore, 632014, India.
Mohammad AfzalDepartment of Pharmaceutical Sciences, Pharmacy Program, Batterjee Medical College, Jeddah, 21442, Saudi Arabia.
Manjunath Mirle RekhaDepartment of Chemistry and Biochemistry, School of Sciences, JAIN (Deemed to Be University), Bengaluru, Karnataka, India.
Samir SahooDepartment of General Medicine, IMS and SUM Hospital, Siksha 'O' Anusandhan (Deemed to be University), Bhubaneswar, India.
Surya Nath PandeyDepartment of Pharmacology, Teerthanker Mahaveer College of Pharmacy, Teerthanker Mahaveer University, Moradabad, India.
Chandana MajiNoida Institute of Engineering and Technology (Pharmacy Institute), 19 Knowledge Park 2, Greater Noida, India.
Kavita GoyalSharda University, Greater Noida, India.
Haider AliDepartment of Pharmacology, Kyrgyz State Medical College, Bishkek, Kyrgyzstan.
Sachin Kumar SinghSchool of Pharmaceutical Sciences, Lovely Professional University, Phagwara, India.
Gaurav GuptaCentre for Research Impact & Outcome, Chitkara College of Pharmacy, Chitkara University, Rajpura, Punjab, India.
Md Sadique HussainUttaranchal Institute of Pharmaceutical Sciences, Uttaranchal University, Dehradun, 248007, Uttarakhand, India.
Purushothaman BalakrishnanTanBio R and D Solution, Thiruvarur, 610103, TamilNadu, India.
Sivakumar ArumugamProtein Engineering Lab, School of Biosciences and Technology, Vellore Institute of Technology, Katpadi, Vellore, 632014, India. siva_kumar.a@vit.ac.in.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Ubiquitination and deubiquitination are biological mechanisms that including the addition and removal ubiquitin molecules from proteins, which are associated with NSCLC. NSCLC is the most common kind of lung cancer, and treatment resistance and cancer development are linked to these alterations. Ubiquitination incorporates proteins by a particular enzyme class, and deubiquitination removes ubiquitins. In NSCLC, this modification is detrimental to cellular function and affects tumorigenesis, apoptosis, and signaling pathways. Conversely, deubiquitination refers to the process through which the ubiquitins are removed from the proteins so that they can perform their functions properly. These processes can be considered therapeutic in some sense, as regulating both can result in an effective therapy for NSCLC. Many studies have been carried out to find potential areas where further drug research could be focused. This study examines the functions of ubiquitination and deubiquitination in NSCLC pathogenesis and resistance, focusing on their mechanisms, consequences, and therapeutic possibilities.

Indexed as

DeubiquitinationNon-small cell lung carcinomaProtein stabilityUbiquitinationUbiquitin ligases

Identifiers

PMID41619095
PMCPMC12936326

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.