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ReviewNaunyn-Schmiedeberg's archives of pharmacology2025

Tumor immune evasion and the Let-7 family: insights into mechanisms and therapies.

Omer Qutaiba B Allela, Ali Fawzi Al-Hussainy, Gaurav Sanghvi, R Roopashree, Aditya Kashyap, D Alex Anand, Rajashree Panigrahi, Lilia Maratovna Garifulina, Sada Ghalib Taher, Mariem Alwan and 2 more

Abstract readReview
PubMed Publisher
In one paragraph

Review in Naunyn-Schmiedeberg's archives of pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

0numbers the graph read from it
0cells of the map it votes in
4citing 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

4 citing papers in PubMed.

  1. Review
  2. Article
  3. Article
  4. 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

12 authors.

Omer Qutaiba B AllelaCollege of Pharmacy, Alnoor University, Mosul, Iraq. omerqba@proton.me.
Ali Fawzi Al-HussainyCollege of Pharmacy, Ahl Al Bayt University, Kerbala, Iraq.
Gaurav SanghviDepartment of Microbiology, Faculty of Science, Marwadi University Research Center, Marwadi University, Rajkot, Gujarat, 360003, India.
R RoopashreeDepartment of Chemistry and Biochemistry, School of Sciences, JAIN (Deemed to be University), Bangalore, Karnataka, India.
Aditya KashyapCentre for Research Impact & Outcome, Chitkara University Institute of Engineering and Technology, Chitkara University, Rajpura, Punjab, 140401, India.
D Alex AnandDepartment of Biomedical, Sathyabama Institute of Science and Technology, Chennai, Tamil Nadu, India.
Rajashree PanigrahiDepartment of Microbiology, IMS and SUM Hospital, Siksha 'O' Anusandhan (Deemed to be University), Bhubaneswar, Odisha, 751003, India.
Lilia Maratovna GarifulinaDepartment of Pediatrics, Samarkand State Medical University, Samarkand, Uzbekistan.
Sada Ghalib TaherCollege of Health and Medical Technology, National University of Science and Technology, Dhi Qar, 64001, Iraq.
Mariem AlwanPharmacy college, Al-Farahidi University, Baghdad, Iraq.
Mahmood JawadDepartment of Pharmacy, Al-Zahrawi University College, Karbala, Iraq.
Hiba MushtaqGilgamesh Ahliya University, Baghdad, Iraq.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Tumor immune evasion is a complex and adaptive mechanism that allows cancer cells to escape immune detection and destruction, contributing to malignancy progression and poor therapeutic outcomes. This review article explores the integral role of the let-7 family of microRNAs (miRNAs) in mediating tumor immune evasion, particularly how these regulators influence the tumor microenvironment (TME) and immune cell functionality. The let-7 family, known for its tumor-suppressive roles, modulates key immune checkpoints, including PD-L1, and pathways linked to immune response regulation, such as the STAT3/SOCS axis, impacts macrophage polarization and modulates immune cell function. Dysregulation of let-7 miRNAs can enhance tumor immune evasion through mechanisms such as downregulating major histocompatibility complex (MHC) expressions, promoting immunosuppressive cell populations, and manipulating metabolic pathways, which together establish an immunosuppressive TME. Conversely, specific let-7 members show potential in restoring anti-tumor immunity by reversing immune suppression and improving T cell responses. By synthesizing current research, this article underscores the dual role of let-7 in both promoting and inhibiting tumor immune evasion, suggesting their potential as therapeutic targets and biomarkers in cancer immunotherapy. Future studies on the context-dependent roles and advanced delivery systems for let-7-targeting therapies are crucial for enhancing immunotherapeutic efficacy and improving patient outcomes across malignancies.

Indexed as

MicroRNAsNeoplasmsTumor EscapeAnimalsAntineoplastic AgentsBiomarkers, TumorGene Expression Regulation, NeoplasticHumansImmune Checkpoint InhibitorsImmune Checkpoint ProteinsImmunotherapyMiceTreatment OutcomeTumor MicroenvironmentAntineoplastic AgentsBiomarkers, TumorImmune Checkpoint InhibitorsImmune Checkpoint ProteinsMicroRNAsmirnlet7 microRNA, humanmirnlet7 microRNA, mouseImmune evasionImmunosuppressive tumor microenvironmentLet-7micoRNATumor microenvironment

Identifiers

What Socratic holds

Textmetadata
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.