Evidence map›Paper›PMID 38698330›Full record

ArticleCellular & molecular biology letters2024

Sesamolin serves as an MYH14 inhibitor to sensitize endometrial cancer to chemotherapy and endocrine therapy via suppressing MYH9/GSK3β/β-catenin signaling.

Yibin Lin, Xiao Chen, Linping Lin, Benhua Xu, Xiaofeng Zhu, Xian Lin

Abstract read
In one paragraph

Article in Cellular & molecular biology letters, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing 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

14 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

6 authors.

Yibin Lin *Department of Gynecology, Clinical Oncology School of Fujian Medical University, Fujian Cancer Hospital, Fuzhou, 350014, Fujian, China.
Xiao Chen *Department of Intensive Care Unit, The First Affiliated Hospital, Fujian Medical University, Fuzhou, 350005, Fujian, China.
Linping LinHunan Institute of Engineering, Xiangtan, 411100, Hunan, China.
Benhua XuDepartment of Radiation Oncology, Fujian Medical University Union Hospital, Xinquan Road 29, Gulou District, Fuzhou, 350001, Fujian, China. benhuaxu@163.com.
Xiaofeng ZhuDepartment of Oral Maxillo-Facial Surgery, The First Affiliated Hospital, Fujian Medical University, No. 20 Chazhong Road, Taijing District, Fuzhou, 350005, Fujian, China. zhuxiaofengfjmu@163.com.
Xian LinShenzhen Key Laboratory of Inflammatory and Immunology Diseases, No. 1120 Lianhua Road, Futian District, Shenzhen, 518036, Guangdong, China. linxiangabriel@fjmu.edu.cn.ORCID http://orcid.org/0000-0001-9043-2648

Funding

Fujian Province Finance Project BPB-ZXF2021Fujian Provincial Financial Health Provincial Special Subsidy Funds BPB-2023ZXFGuangdong Basic and Applied Basic Research Foundation 2021A1515111089Joint Funds for the Innovation of Science and Technology, Fujian Province 2023Y9454Medical Innovation Project of Fujian Provincial Health Commission 2020CXA036Natural Science Foundation of Fujian Province 2021J01233
6 · The paper itself

Abstract

backgroundEndometrial cancer (EC) is one of the most common gynecological cancers. Herein, we aimed to define the role of specific myosin family members in EC because this protein family is involved in the progression of various cancers.

methodsBioinformatics analyses were performed to reveal EC patients' prognosis-associated genes in patients with EC. Furthermore, colony formation, immunofluorescence, cell counting kit 8, wound healing, and transwell assays as well as coimmunoprecipitation, cycloheximide chase, luciferase reporter, and cellular thermal shift assays were performed to functionally and mechanistically analyze human EC samples, cell lines, and a mouse model, respectively.

resultsMachine learning techniques identified MYH14, a member of the myosin family, as the prognosis-associated gene in patients with EC. Furthermore, bioinformatics analyses based on public databases showed that MYH14 was associated with EC chemoresistance. Moreover, immunohistochemistry validated MYH14 upregulation in EC cases compared with that in normal controls and confirmed that MYH14 was an independent and unfavorable prognostic indicator of EC. MYH14 impaired cell sensitivity to carboplatin, paclitaxel, and progesterone, and increased cell proliferation and metastasis in EC. The mechanistic study showed that MYH14 interacted with MYH9 and impaired GSK3β-mediated β-catenin ubiquitination and degradation, thus facilitating the Wnt/β-catenin signaling pathway and epithelial-mesenchymal transition. Sesamolin, a natural compound extracted from Sesamum indicum (L.), directly targeted MYH14 and attenuated EC progression. Additionally, the compound disrupted the interplay between MYH14 and MYH9 and repressed MYH9-regulated Wnt/β-catenin signaling. The in vivo study further verified sesamolin as a therapeutic drug without side effects.

conclusionsHerein, we identified that EC prognosis-associated MYH14 was independently responsible for poor overall survival time of patients, and it augmented EC progression by activating Wnt/β-catenin signaling. Targeting MYH14 by sesamolin, a cytotoxicity-based approach, can be applied synergistically with chemotherapy and endocrine therapy to eventually mitigate EC development. This study emphasizes MYH14 as a potential target and sesamolin as a valuable natural drug for EC therapy.

Indexed as

beta CateninEndometrial NeoplasmsGlycogen Synthase Kinase 3 betaMyosin Heavy ChainsAnimalsAntineoplastic AgentsCell Line, TumorCell ProliferationFemaleGene Expression Regulation, NeoplasticHumansMiceMice, NudeMiddle AgedNaphthoquinonesPrognosisAntineoplastic Agentsbeta CateninGlycogen Synthase Kinase 3 betaMYH9 protein, humanMyosin Heavy ChainsNaphthoquinonesChemotherapyEndocrine therapyEndometrial cancerMYH14Sesamolin

Identifiers

PMID38698330
PMCPMC11067147

What OpenQuestion holds

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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 OpenQuestion graph.