Ribosomal protein <scp>L5</scp> mediated inhibition of <scp>c‐Myc</scp> is critically involved in sanggenon G induced apoptosis in non‐small lung cancer cells

Park, Ji Eon; Jung, Ji Hoon; Lee, Hyo‐Jung; Sim, Deok Yong; Im, Eunji; Park, Woon Yi; Shim, Bum Sang; Ko, Seong‐Gyu; Kim, Ju‐Ha

doi:10.1002/ptr.6878

Cited by 9 publications

(11 citation statements)

References 30 publications

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“…Guangsangon L (145) − 389.3 [74] M. macroura [74]; M. yunanensis [23] Soroceal B (146) + 137.5 [13] M. alba [13] Soroceal (147) + 365 [90] M. nigra [128]; S. bonplandii [90] Morusalbanol A (148) #…”

Section: Dehydroprenyl-2-arylbenzofuran Type Mdaas (Type A)mentioning

confidence: 99%

Mulberry Diels–Alder-type adducts: isolation, structure, bioactivity, and synthesis

Luo

Zhu

Zou

et al. 2022

Nat. Prod. Bioprospect.

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Mulberry Diels–Alder-type adducts (MDAAs) are unique phenolic natural products biosynthetically derived from the intermolecular [4 + 2]-cycloaddition of dienophiles (mainly chalcones) and dehydroprenylphenol dienes, which are exclusively distributed in moraceous plants. A total of 166 MDAAs with diverse skeletons have been isolated and identified since 1980. Structurally, the classic MDAAs characterized by the chalcone-skeleton dienophiles can be divided into eight groups (Types A − H), while others with non-chalcone dienophiles or some variations of classic MDAAs are non-classic MDAAs (Type I). These compounds have attracted significant attention of natural products and synthetic chemists due to their complex architectures, remarkable biological activities, and synthetic challenges. The present review provides a comprehensive summary of the structural properties, bioactivities, and syntheses of MDAAs. Cited references were collected between 1980 and 2021 from the SciFinder, Web of Science, and China National Knowledge Internet (CNKI). Graphical Abstract

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Section: Dehydroprenyl-2-arylbenzofuran Type Mdaas (Type A)mentioning

confidence: 99%

Mulberry Diels–Alder-type adducts: isolation, structure, bioactivity, and synthesis

Luo

Zhu

Zou

et al. 2022

Nat. Prod. Bioprospect.

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“…Numerous studies have reported that RPL5 was involved in the progression of various malignant tumors [6][7][8][9]. The pan-cancer gene expression patterns were performed to examine the differential expression of RPL5 across TCGA cancer types.…”

Section: Rpl5 Expression In Normal Tissues and Pan-cancermentioning

confidence: 99%

“…The ribosomal protein RPL5 is a component of the ribosome, a large ribonucleoprotein complex responsible for protein synthesis in cells. RPL5 is involved in the development and progression of a variety of tumors, such as melanoma [6], liver cancer [7], breast cancer [8], and non-small cell lung cancer [9]. However, the role and regulation mechanism of RPL5 has not been revealed in colon cancer.…”

Section: Introductionmentioning

confidence: 99%

Ribosomal protein RPL5 regulates colon cancer cell proliferation and migration through MAPK/ERK signaling pathway

Zhang

Dang

Wang

et al. 2022

Preprint

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Background: Abnormal expression of ribosomal proteins has an important regulatory effect on the progression of cancer. RPL5 is involved in the progression of various malignancies, however, the role of RPL5 in colon cancer remains is still unclear. Methods: Data from TCGA and GTEx databases were used to analyze the RPL5 expression in pan-cancer. The expression level of RPL5 in clinical colon cancer tissue samples and human colon cancer cell lines was detected by western blotting; siRNA targeting RPL5 was designed, and its interference efficiency was verified by western blotting and RT-qPCR; CCK8 assay, clone formation assay, cell cycle assay, and cell scratch assay were used to observe the effect of RPL5 on colon cancer cell proliferation and migration; the changes of proteins related to MAPK/ERK signaling pathway were also detected using western blotting. Results: The expression level of RPL5 in colon cancer tissues and cell lines was significantly higher than that in adjacent tissues and NCM460 cells, respectively, and its expression level was higher in HCT116 cells and RKO cells. Knockdown of RPL5 significantly inhibited the proliferation and migration of HCT16 and RKO cells, and arrested the cell cycle in G0/G1 phase. Mechanistic studies revealed that the expression of p-MEK1/2, p-ERK, c-Myc were down-regulated, and the expression of FOXO3 was up-regulated after down-regulation of RPL5, ERK activator (TBHQ) could partially reverse the above-mentioned effects caused by siRPL5. Moreover, TBHQ could partially reverse the inhibitory effect of siRPL5 on the proliferation and migration of colon cancer cells. Collectively, RPL5 promoted colon cell proliferation and migration, at least in part, by activating the MAPK/ERK signaling pathway.Conclusion: RPL5 promoted colon cell proliferation and migration, at least in part, by activating the MAPK/ERK signaling pathway, which may serve as a novel therapeutic target for cancers in which MAPK/ERK signaling is a dominant feature.

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“…Based on Park et al's paper [6], to detect cell death, HCT116 or SW480 cells were treated with Morusin (5 µM) for 24 h, and incubated with TUNEL assay mixture for 60 min by using the DeadEnd™ Fluorometric TUNEL system kit (Promega, Madison, WI, USA).…”

Section: Tunel Assaymentioning

confidence: 99%

“…It is well documented that c-Myc is a biomarker for poor prognosis of CRC patients, as it is a transcription factor that is critically associated with cell growth, cell adhesion, proliferation, and apoptosis [6]. Hence, to target c-Myc has been considered a good strategy for prevention or treatment of CRCs [7].…”

Section: Introductionmentioning

confidence: 99%

miR193a-5p Mediated ZNF746 and c-Myc Signaling Axis Is Critically Involved in Morusin Induced Apoptosis in Colorectal Cancer Cells

Park

Lee

Sim

et al. 2021

Cells

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Novel target therapy is on the spotlight for effective cancer therapy. Hence, in the present study, the underlying apoptotic mechanism of Morusin was explored in association with miR193a-5p mediated ZNF746/c-Myc signaling axis in colorectal cancer cells (CRCs). Herein, Morusin reduced the viability and the number of colonies in HCT116 and SW480 CRCs. Additionally, Morusin increased sub-G1 population, cleavages of poly (ADP-ribose) polymerase (PARP) and caspase-3 and inhibited the expression of zinc finger protein 746 (ZNF746) and c-Myc in HCT116 and SW480 cells. Conversely, overexpression of ZNF746 suppressed the ability of Morusin to abrogate the expression of c-Myc in HCT116 cells, as ZNF746 enhanced the stability of c-Myc via their direct binding through nuclear colocalization in HCT116 cells by immunofluorescence and immunoprecipitation. Notably, Morusin upregulated miR193a-5p as a tumor suppressor, while miR193a-5p inhibitor masked the ability of Morusin to reduce the expression of ZNF746, c-Myc, and pro-PARP in HCT116 cells. To our knowledge, these findings provide the novel insight on miR193a-5p mediated inhibition of ZNF746/c-Myc signaling in Morusin induced apoptosis in CRCs.

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Ribosomal protein L5 mediated inhibition of c‐Myc is critically involved in sanggenon G induced apoptosis in non‐small lung cancer cells

Cited by 9 publications

References 30 publications

Mulberry Diels–Alder-type adducts: isolation, structure, bioactivity, and synthesis

Mulberry Diels–Alder-type adducts: isolation, structure, bioactivity, and synthesis

Ribosomal protein RPL5 regulates colon cancer cell proliferation and migration through MAPK/ERK signaling pathway

miR193a-5p Mediated ZNF746 and c-Myc Signaling Axis Is Critically Involved in Morusin Induced Apoptosis in Colorectal Cancer Cells

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