Evidence map›Paper›PMID 40804316›Full record

ArticleScientific reports2025

LINC00162 silencing enhances sorafenib sensitivity and inhibits thyroid cancer cells progression through modulation of MAPK signaling and apoptosis.

Maryam Hejazi, Seyedeh Zahra Bahojb Mahdavi, Saba Abedimanesh, Ramin Heshmat, Bagher Larijani, Amir Ali Mokhtarzadeh, Gita Shafiee, Seyed Mohammad Tavangar

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In one paragraph

Article in Scientific reports, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing 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

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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

9 citing papers in PubMed.

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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.

Maryam HejaziChronic Diseases Research Center, Endocrinology and Metabolism Population Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran.
Seyedeh Zahra Bahojb MahdaviImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Saba AbedimaneshImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran.
Ramin HeshmatChronic Diseases Research Center, Endocrinology and Metabolism Population Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran.
Bagher LarijaniEndocrinology and Metabolism Research Center, Endocrinology and Metabolism Clinical Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran.
Amir Ali MokhtarzadehImmunology Research Center, Tabriz University of Medical Sciences, Tabriz, Iran. ahad.mokhtarzadeh@gmail.com.
Gita ShafieeChronic Diseases Research Center, Endocrinology and Metabolism Population Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran. gshafee.endocrine@gmail.com.
Seyed Mohammad TavangarChronic Diseases Research Center, Endocrinology and Metabolism Population Sciences Institute, Tehran University of Medical Sciences, Tehran, Iran. tavangar@ams.ac.ir.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Many studies have reported the aberrant expression of lncRNAs and indicated their role in cancer progression and drug resistance across various cancers. In this study, we aimed to evaluate the effect of LINC00162 lncRNA on the chemosensitivity of thyroid cancer cells, both individually and in combination with sorafenib, on various biological processes. In this regard, we conducted our experiments in several groups: (1) LINC00162 siRNA-transfected cells, (2) Sorafenib-treated cells, (3) Cells that received both siRNA transfection and sorafenib treatment (4) Control group. MTT assay results revealed that siRNA-mediated silencing of LINC00162 reduced the viability of the B-CPAP thyroid cancer cells and increased the sensitivity of these cells to sorafenib by reducing its IC50. Flow cytometry analysis of apoptosis and cell cycle progression indicated that LINC00162 silencing induced apoptosis and Sub-G1 cell cycle arrest, while its combination with sorafenib significantly increased the apoptosis rate and also arrested cells in the G2-M phase in addition to the Sub-G1 phase. This combination treatment increased the expression of apoptosis-related genes BAX, CASP3, CASP9 while decreasing BCL2 expression. Additionally, significant inhibition of the cell-cycle related genes MYC and Cyclin D and upregulation of TP53 were observed following combination treatment. Furthermore, the combination therapy reduced the migration of B-CPAP cells through the downregulation of MMP-3 and MMP-9. Colony sizes and numbers also decreased following siRNA-mediated silencing of LINC00162 and sorafenib treatment. qRT-PCR analysis of stemness-related genes, including NANOG, SOX2, CD44, and CD133 confirmed the findings of the colony formation assay. To understand the underlying mechanisms of LINC00162 lncRNA in thyroid cancer progression, we evaluated the expression of MAPK pathway genes. Our findings indicated that LINC00162 silencing, in combination with sorafenib, reduced the expression of MAPK, KRAS, and RAF genes. From our findings, we can conclude that LINC00162 silencing, both individually and combined with sorafenib, reduced the progression and viability of thyroid cancer cells through modulating genes involved in key pathways and could be considered a new therapeutic approach for the treatment of papillary thyroid cancer (PTC).

Indexed as

ApoptosisMAP Kinase Signaling SystemRNA, Long NoncodingSorafenibThyroid NeoplasmsAntineoplastic AgentsCell Line, TumorCell ProliferationDisease ProgressionDrug Resistance, NeoplasmGene Expression Regulation, NeoplasticGene SilencingHumansRNA, Small InterferingAntineoplastic AgentsRNA, Long NoncodingRNA, Small InterferingSorafenibApoptosisAutophagyChemosensitivityLINC00162LncRNAMAPK pathwaySorafenibThyroid Cancer

Identifiers

PMID40804316
PMCPMC12350744

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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.