Kazinol-E is a specific inhibitor of ERK that suppresses the enrichment of a breast cancer stem-like cell population

Jung, Yuchae; Han, Seula; Li, Hua; Ahn, Yeon-Hwa; Cho, Hyewon; Lee, Cheol-Jung; Lee, Hani; Cho, Yong‐Yeon; Ryu, Jae‐Ha; Jeon, Raok; Kim, Woo Young

doi:10.1016/j.bbrc.2016.01.066

Cited by 24 publications

(15 citation statements)

References 29 publications

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“…Bioinformatics screening indicated MAPK1 served as a target of miR-326. MAPK1, mitogen-activated protein kinase 1, belongs to MAP kinase family and is a key member of MAPK/ERK pathway [22, 23]. It widely participates in various pathological processes of cancer cells, including cell proliferation, migration, cell differentiation, cell survival and apoptosis [24].…”

Section: Introductionmentioning

confidence: 99%

The lncRNA TDRG1 promotes cell proliferation, migration and invasion by targeting miR-326 to regulate MAPK1 expression in cervical cancer

et al. 2019

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Background Recently, lncRNA-Testis developmental related gene 1 (TDRG1) was proved to be a key modulator in reproductive organ-related cancers. The biological role of TDRG1 in cervical cancer (CC) progression remains largely unknown. Method Real-time PCR (qRT-PCR) examined the expression level of TDRG1, microRNA (miR)-326 and MAPK1 mRNA. OS tissues and corresponding relative normal tissues, as well as CC cell lines and normal cell line Ect1/E6E7 were collected to determine the expression of TDRG1 in CC. MTT, colony formation, wound-healing, transwell and flow cytometer assay detected the influence of TDRG1 and miR-326 on CC cells growth, metastasis and apoptosis. Western blot examined proteins level. Bioinformatics, RNA pull-down assay, RNA immunoprecipitation and dual-luciferase reporter assays detected the molecular mechanism of TDRG1 in CC. Xenograft tumour model was established to determine the role of TDRG1 in vivo. Results The expression of TDRG1 was significantly increased in CC tissues and cell lines compared with normal tissue and normal cell line respectively and its expression was associated with clinicopathological characteristics of CC patients. Knockdown of TDRG1 inhibited the cell proliferation, migration and invasion in Hela and SIHA cells. Moreover, TDRG1 directly interacted with miR-326, and the inhibition effect on cell growth and metastasis induced by TDRG1 siRNA can be abrogated by miR-326 silencing by its inhibitor in Hela and SIHA cells. Further, MAPK1 was proved to be a direct target of miR-326, and its expression was negatively regulated by miR-326 while positively modulated by TDRG1. Conclusion TDRG1 acts as a competing endogenous lncRNA (ceRNA) to modulate MAPK1 by sponging miR-326 in CC, shedding new light on TDRG1-directed diagnostics and therapeutics in CC.

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Section: Introductionmentioning

confidence: 99%

The lncRNA TDRG1 promotes cell proliferation, migration and invasion by targeting miR-326 to regulate MAPK1 expression in cervical cancer

et al. 2019

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“…Mitogen-activated protein kinase 1 ( MAPK1 ) belongs to the MAP kinase family. MAP kinase, also known as extracellular signal-regulated kinases (ERKs), could act as a binding point for numerous biochemical signals [ 19 , 20 ]. Besides, ERKs are also involved in a wide range of cellular processes, such as differentiation, proliferation, transcription development and regulation [ 21 ].…”

Section: Introductionmentioning

confidence: 99%

MiR-143 inhibits endometrial cancer cell proliferation and metastasis by targetingMAPK1

et al. 2017

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Endometrial cancer (EC) is one of the most commonly diagnosed gynecologic malignancies in the world, with the morbidity rate of over 7%. The mechanism of the pathogenesis has not been specifically elucidated to date, which is imperative for EC treatment. The aim of our study was to investigate the target relationship between miR-143 and mitogen-activated protein kinase 1 (MAPK1) and explore the effect of miR-143 on the endometrial cancers (EC) cells through targeting MAPK1. We collected EC tissues and adjacent tissues, and transfected miR-143 mimics and MAPK1 siRNA into EC cells with lipofectamine. Reverse transcription-polymerase chain reaction (RT-PCR) and western blot were used to examine the expression of miR-143 and MAPK1 mRNA and the protein expression of MAPK1. Cell counting kit-8, wound healing assay, flow cytometry and transwell assay were applied to examining the alteration of the proliferation, migration, cell cycle and invasion ability of EC cells. We predicted the targeting gene of miR-143 through bioinformatics analysis. MiR-143 was found under-expressed in EC tissues and cells. Overexpression of miR-143 or knockdown of MAPK1 in human EC cell line HEC-1B inhibited the EC cell proliferation, migration and invasion and induced apoptosis. MAPK1 was verified to be a target gene of miR-143. MiR-143 overexpression could effectively inhibit mRNA and protein expression of MAPK1 in HEC-1B cells. Collectively, miR-143 might inhibit the proliferation, migration and invasion of EC cells, and promote the apoptosis of EC cells by suppressing MAPK1. These findings provided a view for new and potential therapeutic method for the clinical treatment of EC.

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“…In the groups treated with AC009 alone or with AC009 combined with cetuximab, the CD44 + /CD24 + CSCs significantly decreased to 18.2% and 14.5%, respectively. Because ERK inhibitors may suppress the enrichment of breast cancer stem-like cell populations [21], we also determined whether the ERK pathway was involved in AC009-treated HCT116 cells. ERK activation was abolished by AC009 (Figure 7C).…”

Section: Resultsmentioning

confidence: 99%

Novel Antrodia cinnamomea Extract Reduced Cancer Stem-Like Phenotype Changes and Resensitized KRAS-Mutant Colorectal Cancer via a MicroRNA-27a Pathway

Lin

Lai

Lee

et al. 2019

Cancers

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Colorectal cancer (CRC) is one of the most common causes of death in Taiwan. Previous studies showed that Antrodia cinnamomea (AC) can treat poisoning, diarrhea, and various types of cancer. Therefore, we purified a novel ubiquinone derivative, AC009, and investigated its antitumor effects. Cell viability assays revealed that AC009 reduced the viability of several human CRC cell lines. AC009 treatment resulted in cell-cycle arrest/apoptosis, and these effects may occur via caspase and Bcl-2 signaling pathways. We demonstrated that AC009 could significantly inhibit in vivo tumor growth in xenograft mouse models. Using messenger RNA (mRNA) and microRNA (miRNA) microarrays, we found that KRAS gene expression was also regulated by AC009, possibly through specific miRNAs. AC009 also reduced cancer stem-cell marker CD44+/CD24+ expression and restored the tumor inhibition effect of cetuximab in KRAS-mutant CRC. Moreover, we found that miRNA-27a could restore the tumor inhibition effect of cetuximab in KRAS-mutant CRC cells. Taken together, our results suggest that AC009 has therapeutic potential against human wild-type and KRAS-mutant CRC.

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Kazinol-E is a specific inhibitor of ERK that suppresses the enrichment of a breast cancer stem-like cell population

Cited by 24 publications

References 29 publications

The lncRNA TDRG1 promotes cell proliferation, migration and invasion by targeting miR-326 to regulate MAPK1 expression in cervical cancer

The lncRNA TDRG1 promotes cell proliferation, migration and invasion by targeting miR-326 to regulate MAPK1 expression in cervical cancer

MiR-143 inhibits endometrial cancer cell proliferation and metastasis by targetingMAPK1

Novel Antrodia cinnamomea Extract Reduced Cancer Stem-Like Phenotype Changes and Resensitized KRAS-Mutant Colorectal Cancer via a MicroRNA-27a Pathway

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