Evidence map›Paper›PMID 36872049›Full record

ArticleZhongguo fei ai za zhi = Chinese journal of lung cancer2023

[Study on the Biological Function of Abemecilib in Inhibiting the Proliferation, Invasion and
Migration of Small Cell Lung Cancer with High c-Myc Expression].

Jingjing Guo, Di Mu, Wenwen Yu, Leina Sun, Jiali Zhang, Xiubao Ren, Ying Han

Erratum issuedOpen access · greenFull text readEnglish Abstract
In one paragraph

Article in Zhongguo fei ai za zhi = Chinese journal of lung cancer, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. 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

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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 citations in OpenAlex.

  1. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

7 authors at 1 institution in 1 country.

Jingjing GuoDepartment of Immunology, Tianjin Medical University Cancer Institute and Hospital; National Clinical Research Center for Cancer; Tianjin Key Laboratory of Cancer Prevention and Therapy; Tianjin's Clinical Research Center for Cancer; Tianjin Key Laboratory of Cancer Immunology and Biotherapy, Tianjin 300060, China.
Di MuDepartment of Immunology, Tianjin Medical University Cancer Institute and Hospital; National Clinical Research Center for Cancer; Tianjin Key Laboratory of Cancer Prevention and Therapy; Tianjin's Clinical Research Center for Cancer; Tianjin Key Laboratory of Cancer Immunology and Biotherapy, Tianjin 300060, China.
Wenwen YuDepartment of Immunology, Tianjin Medical University Cancer Institute and Hospital; National Clinical Research Center for Cancer; Tianjin Key Laboratory of Cancer Prevention and Therapy; Tianjin's Clinical Research Center for Cancer; Tianjin Key Laboratory of Cancer Immunology and Biotherapy, Tianjin 300060, China.
Leina SunDepartment of Pathology, Tianjin Medical University Cancer Institute and Hospital; National Clinical Research Center for Cancer; Tianjin Key Laboratory of Cancer Prevention and Therapy; Tianjin's Clinical Research Center for Cancer; Tianjin Key Laboratory of Cancer Immunology and Biotherapy, Tianjin 300060, China.
Jiali ZhangDepartment of Biotherapy, Tianjin Medical University Cancer Institute and Hospital; National Clinical Research Center for Cancer; Tianjin Key Laboratory of Cancer Prevention and Therapy; Tianjin's Clinical Research Center for Cancer; Tianjin Key Laboratory of Cancer Immunology and Biotherapy, Tianjin 300060, China.
Xiubao RenDepartment of Immunology, Tianjin Medical University Cancer Institute and Hospital; National Clinical Research Center for Cancer; Tianjin Key Laboratory of Cancer Prevention and Therapy; Tianjin's Clinical Research Center for Cancer; Tianjin Key Laboratory of Cancer Immunology and Biotherapy, Tianjin 300060, China.
Ying HanDepartment of Immunology, Tianjin Medical University Cancer Institute and Hospital; National Clinical Research Center for Cancer; Tianjin Key Laboratory of Cancer Prevention and Therapy; Tianjin's Clinical Research Center for Cancer; Tianjin Key Laboratory of Cancer Immunology and Biotherapy, Tianjin 300060, China.
Tianjin Medical University Cancer Institute and Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundSmall cell lung cancer (SCLC) with high c-Myc expression is prone to relapse and metastasis, leading to extremely low survival rate. Cyclin-dependent kinases 4 and 6 (CDK4/6) inhibitor Abemaciclib plays a key role in the treatment of tumors, but the effects and mechanisms on SCLC remain unclear. This study was to analyze the effect and molecular mechanism of Abemaciclib in inhibiting proliferation, migration and invasion of SCLC with high c-Myc expression, with a view to expanding a new direction for reducing the recurrence and metastasis.

methodsProteins interacting with CDK4/6 were predicted using the STRING database. The expressions of CDK4/6 and c-Myc in 31 cases of SCLC cancer tissues and paired adjacent normal tissues were analyzed by immunohistochemistry. The effects of Abemaciclib on the proliferation, invasion and migration of SCLC were detected by CCK-8, colony formation assay, Transwell and migration assay. Western blot was used to detect the expressions of CDK4/6 and related transcription factors. Flow cytometry was used to analyze the effects of Abemaciclib on the cell cycle and checkpoint of SCLC.

resultsThe expression of CDK4/6 was associated with c-Myc by STRING protein interaction network. c-Myc can directly modalize achaete-scute complex homolog 1 (ASCL1), neuronal differentiation 1 (NEUROD1) and Yes-associated protein 1 (YAP1). Moreover, CDK4 and c-Myc regulate the expression of programmed cell death ligand 1 (PD-L1). Immunohistochemistry showed that the expressions of CDK4/6 and c-Myc in cancer tissues were higher than those in adjacent tissues(P<0.0001). CCK-8, colony formation assay, Transwell and migration assay verified that Abemaciclib could effectively inhibit the proliferation, invasion and migration of SBC-2 and H446OE(P<0.0001). Western blot analysis further showed that Abemaciclib not only inhibited CDK4 (P<0.05) and CDK6 (P<0.05), but also affected c-Myc (P<0.05), ASCL1 (P<0.05), NEUROD1 (P<0.05) and YAP1 (P<0.05), which are related to SCLC invasion and metastasis. Flow cytometry showed that Abemaciclib not only inhibited the cell cycle progression of SCLC cells (P<0.0001), but also significantly increased PD-L1 expression on SBC-2 (P<0.01) and H446OE (P<0.001).

conclusionsAbemaciclib significantly inhibits the proliferation, invasion, migration and cell cycle progression of SCLC by inhibiting the expressions of CDK4/6, c-Myc, ASCL1, YAP1 and NEUROD1. Abemaciclib can also increase the expression of PD-L1 in SCLC.

Indexed as

Lung NeoplasmsSmall Cell Lung CarcinomaAdaptor Proteins, Signal TransducingAminopyridinesB7-H1 AntigenBenzimidazolesCell ProliferationHumansNeoplasm Recurrence, LocalSincalideTranscription FactorsabemaciclibAdaptor Proteins, Signal TransducingAminopyridinesB7-H1 AntigenBenzimidazolesSincalideTranscription Factorsc-MycCyclin-dependent kinases 4 and 6Lung neoplasms

Identifiers

PMID36872049
PMCPMC10033240
OpenAlexW4323294644

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LicenceCC BY
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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.