Evidence map›Paper›PMID 35606602›Full record

ArticleMolecular and cellular biochemistry2022

FAT1 downregulation enhances stemness and cisplatin resistance in esophageal squamous cell carcinoma.

Yuanfang Zhai, Chengyuan Shan, Haoyu Zhang, Pengzhou Kong, Ling Zhang, Yanqiang Wang, Xiaoling Hu, Xiaolong Cheng

Abstract read
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In one paragraph

Article in Molecular and cellular biochemistry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
2.7field-weighted citation impact, top 9% of its field
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

16 citing papers in PubMed, 26 citations in OpenAlex.

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  15. The diverse functions of FAT1 in cancer progression: good, bad, or ugly?Journal of experimental & clinical cancer research : CR · 2022
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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 at 1 institution in 1 country.

Yuanfang Zhai *Key Laboratory of Cellular Physiology of the Ministry of Education, Shanxi Medical University, 56 Xin Jian Nan Road, Taiyuan, 030001, Shanxi, People's Republic of China.
Chengyuan Shan *Key Laboratory of Cellular Physiology of the Ministry of Education, Shanxi Medical University, 56 Xin Jian Nan Road, Taiyuan, 030001, Shanxi, People's Republic of China.
Haoyu ZhangKey Laboratory of Cellular Physiology of the Ministry of Education, Shanxi Medical University, 56 Xin Jian Nan Road, Taiyuan, 030001, Shanxi, People's Republic of China.
Pengzhou KongKey Laboratory of Cellular Physiology of the Ministry of Education, Shanxi Medical University, 56 Xin Jian Nan Road, Taiyuan, 030001, Shanxi, People's Republic of China.
Ling ZhangKey Laboratory of Cellular Physiology of the Ministry of Education, Shanxi Medical University, 56 Xin Jian Nan Road, Taiyuan, 030001, Shanxi, People's Republic of China.
Yanqiang WangKey Laboratory of Cellular Physiology of the Ministry of Education, Shanxi Medical University, 56 Xin Jian Nan Road, Taiyuan, 030001, Shanxi, People's Republic of China.
Xiaoling HuKey Laboratory of Cellular Physiology of the Ministry of Education, Shanxi Medical University, 56 Xin Jian Nan Road, Taiyuan, 030001, Shanxi, People's Republic of China. huxiaoling@sxmu.edu.cn.
Xiaolong ChengKey Laboratory of Cellular Physiology of the Ministry of Education, Shanxi Medical University, 56 Xin Jian Nan Road, Taiyuan, 030001, Shanxi, People's Republic of China. chengxl@sxmu.edu.cn.ORCID http://orcid.org/0000-0001-8726-5631
Shanxi Medical University · CN

Funding

National Natural Science Foundation of China 81802825
6 · The paper itself

Abstract

Primary or acquired drug resistance accounts for the failure of chemotherapy and cancer recurrence in esophageal squamous cell carcinoma (ESCC). However, the aberrant mechanisms driving drug resistance are not fully understood in ESCC. In our previous study, FAT Atypical Cadherin 1 (FAT1) was found to inhibit the epithelial-mesenchymal transition (EMT) process in ESCC. EMT plays a critical role in the development of drug resistance in multiple cancer types. Besides, it equips cancer cells with cancer stem cell (CSC)-like characters that also are associated with chemotherapy resistance. Whether FAT1 regulates the stemness or drug resistance of ESCC cells is worth being explored. Here we found that FAT1 was downregulated in ESCC spheres and negatively correlated with stemness-associated markers including ALDH1A1 and KLF4. Knocking down FAT1 enhanced the sphere-forming ability, resistance to cisplatin and drug efflux of ESCC cells. Additionally, FAT1 knockdown upregulated the expression of drug resistance-related gene ABCC3. Furtherly, we found FAT1 knockdown induced the translocation of β-catenin into nucleus and enhanced its transcriptional activity. The result of ChIP showed that β-catenin was enriched in ABCC3 promoter. Furthermore, β-catenin promoted expression of ABCC3. In conclusion, FAT1 knockdown might enhance the stemness and ABCC3-related cisplatin resistance of ESCC cells via Wnt/β-catenin signaling pathway. FAT1 and its downstream gene ABCC3 might be potential targets for overcoming chemoresistance in ESCC.

Indexed as

CadherinsDrug Resistance, NeoplasmEsophageal NeoplasmsEsophageal Squamous Cell CarcinomaNeoplastic Stem Cellsbeta CateninCell Line, TumorCell ProliferationCisplatinDown-RegulationEpithelial-Mesenchymal TransitionGene Expression Regulation, NeoplasticHumansbeta CateninCadherinsCisplatinFAT1 protein, humanABCC3ESCCFAT1β-Catenin

Identifiers

PMID35606602
OpenAlexW4281387481

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Read underepoch 390

Registered trials

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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.