Evidence map›Paper›PMID 40512336›Full record

ArticleDiscover oncology2025

Glutamate activates the MAPK pathway by inhibiting LPAR1 expression and promotes anlotinib resistance in thyroid cancer.

Bin Liu, Ying Peng, Yanjun Su, Chang Diao, Liansheng Cha, Ruochuan Cheng

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Discover oncology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

6 authors.

Bin Liu *Thyroid Disease Diagnosis and Treatment Center, First Affiliated Hospital of Kunming Medical University, No.295 Xichang Road, Wuhua District, Kunming, 650032, Yunnan, China.
Ying Peng *Thyroid Disease Diagnosis and Treatment Center, First Affiliated Hospital of Kunming Medical University, No.295 Xichang Road, Wuhua District, Kunming, 650032, Yunnan, China.
Yanjun SuThyroid Disease Diagnosis and Treatment Center, First Affiliated Hospital of Kunming Medical University, No.295 Xichang Road, Wuhua District, Kunming, 650032, Yunnan, China.
Chang DiaoThyroid Disease Diagnosis and Treatment Center, First Affiliated Hospital of Kunming Medical University, No.295 Xichang Road, Wuhua District, Kunming, 650032, Yunnan, China.
Liansheng ChaZhenxiong County People's Hospital, Zhaotong , 657216, Yunnan, China.
Ruochuan ChengThyroid Disease Diagnosis and Treatment Center, First Affiliated Hospital of Kunming Medical University, No.295 Xichang Road, Wuhua District, Kunming, 650032, Yunnan, China. cruochuan2023@163.com.

Funding

National Natural Science Foundation of China 82160462
6 · The paper itself

Abstract

objectiveTo investigate the effects of glutamate on thyroid cancer (TC) cell lines and TC-anlotinib-resistant cell lines and to explore the potential molecular mechanism of glutamate and LPAR1 in promoting anlotinib resistance in TC.

methodsGlutamate was used to treat TC cell lines and TC-anlotinib-resistant cell lines, and changes in cell function and effects on the expression of LPAR1 and MAPK pathway-related proteins were assessed. In addition, overexpressed-LPAR1. (OE-LPAR1) cell lines were constructed, and OE-LPAR1 and glutamate were combined with TC cell lines and TC-anlotinib-resistant cell lines to explore the interaction between glutamate and LPAR1. Finally, a xenograft tumor model was established in nude mice, and the protein expression of key nodes was detected for further verification.

resultsGlutamate promoted the migration, invasion and proliferation of TC cell lines and TC-anlotinib-resistant cell lines, inhibited the expression of LPAR1, and promoted the expression of MAPK pathway-related proteins, whereas OE-LPAR1 had the opposite effect. Furthermore, glutamate promoted the expression of Ki67, inhibited apoptosis, significantly inhibited the expression of LPAR1, and promoted the expression of MAPK pathway-related proteins in a nude mouse xenograft tumor model, whereas OE-LPAR1 significantly inhibited the expression of Ki67 and promoted apoptosis.

conclusionOur study revealed that glutamate promotes the progression of malignant biological behavior in TC cell lines and TC-anlotinib-resistant cell lines. Additionally, glutamate may activate the MAPK pathway by inhibiting the expression of LPAR1, thereby promoting resistance to anlotinib in TC.

Indexed as

AnlotinibDrug resistanceGlutamateThyroid cancer

Identifiers

PMID40512336
PMCPMC12165934

What Socratic holds

Textmetadata
LicenceCC BY
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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.