Silibinin suppresses epithelial–mesenchymal transition in human non-small cell lung cancer cells by restraining RHBDD1

Xu, Suyan; Zhang, Hongyan; Wang, Aifeng; Ma, Yongcheng; Gao, Yuan; Li, Guofeng

doi:10.1186/s11658-020-00229-6

Cited by 21 publications

(19 citation statements)

References 46 publications

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“…EMT is critical process during tumor progression and metastasis in which epithelial cells gain mesenchymal features to have better abilities for invasion. This process is characterized by E-cadherin downregulation and vimentin upregulation [108][109][110]. The WNT signaling pathway regulates cell proliferation, polarity and death during embryogenesis [111].…”

Section: Wnt and Hedgehog Signaling Pathwaysmentioning

confidence: 99%

Molecular interactions of miR-338 during tumor progression and metastasis

Moghbeli

2021

Cell Mol Biol Lett

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Background Cancer, as one of the main causes of human deaths, is currently a significant global health challenge. Since the majority of cancer-related deaths are associated with late diagnosis, it is necessary to develop minimally invasive early detection markers to manage and reduce mortality rates. MicroRNAs (miRNAs), as highly conserved non-coding RNAs, target the specific mRNAs which are involved in regulation of various fundamental cellular processes such as cell proliferation, death, and signaling pathways. MiRNAs can also be regulated by long non-coding RNAs (lncRNAs) and circular RNAs (circRNAs). They are highly stable in body fluids and have tumor-specific expression profiles, which suggest their suitability as efficient non-invasive diagnostic and prognostic tumor markers. Aberrant expression of miR-338 has been widely reported in different cancers. It regulates cell proliferation, migration, angiogenesis, and apoptosis in tumor cells. Main body In the present review, we have summarized all miR-338 interactions with other non-coding RNAs (ncRNAs) and associated signaling pathways to clarify the role of miR-338 during tumor progression. Conclusions It was concluded that miR-338 mainly functions as a tumor suppressor in different cancers. There were also significant associations between miR-338 and other ncRNAs in tumor cells. Moreover, miR-338 has a pivotal role during tumor progression using the regulation of WNT, MAPK, and PI3K/AKT signaling pathways. This review highlights miR-338 as a pivotal ncRNA in biology of tumor cells.

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Section: Wnt and Hedgehog Signaling Pathwaysmentioning

confidence: 99%

Molecular interactions of miR-338 during tumor progression and metastasis

Moghbeli

2021

Cell Mol Biol Lett

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“…A drug could be considered for anticancer studies if it can act on some of the hallmarks of cancer, including proliferative signaling, resistance to cell death, evasion of growth suppressors, induction of replicative immortality, initiation of angiogenesis, and stimulation of invasion and metastasis [ 19 ]. The anticancer ability of silibinin against lung cancer is well known [ 36 , 37 ] and our results also showed that increasing concentrations of silibinin induced cell death in NSCLC cells (A549, H292, and H460) [ 28 ].…”

Section: Discussionmentioning

confidence: 65%

Silibinin Regulates Tumor Progression and Tumorsphere Formation by Suppressing PD-L1 Expression in Non-Small Cell Lung Cancer (NSCLC) Cells

Rugamba

Kang

et al. 2021

Cells

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Recently, natural compounds have been used globally for cancer treatment studies. Silibinin is a natural compound extracted from Silybum marianum (milk thistle), which has been suggested as an anticancer drug through various studies. Studies on its activity in various cancers are undergoing. This study demonstrated the molecular signaling behind the anticancer activity of silibinin in non-small cell lung cancer (NSCLC). Quantitative real-time polymerase chain reaction and Western blotting analysis were performed for molecular signaling analysis. Wound healing assay, invasion assay, and in vitro angiogenesis were performed for the anticancer activity of silibinin. The results indicated that silibinin inhibited A549, H292, and H460 cell proliferation in a concentration-dependent manner, as confirmed by the induction of G0/G1 cell cycle arrest and apoptosis and the inhibition of tumor angiogenesis, migration, and invasion. This study also assessed the role of silibinin in suppressing tumorsphere formation using the tumorsphere formation assay. By binding to the epidermal growth factor receptor (EGFR), silibinin downregulated phosphorylated EGFR expression, which then inhibited its downstream targets, the JAK2/STAT5 and PI3K/AKT pathways, and thereby reduced matrix metalloproteinase, PD-L1, and vascular endothelial growth factor expression. Binding analysis demonstrated that STAT5 binds to the PD-L1 promoter region in the nucleus and silibinin inhibited the STAT5/PD-L1 complex. Altogether, silibinin could be considered as a candidate for tumor immunotherapy and cancer stem cell-targeted therapy.

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“…Silencing of RHBDD1 can inhibit cell proliferation and growth in glioblastoma, colorectal, breast cancer, and hepatocellular carcinoma. Silybin inhibits the epithelial‐mesenchymal transformation of NSCLC cells by inhibiting RHBDD1 and exerts anti‐tumor effects on NSCLC cells 241 . Reverse inducible cysteine‐rich protein with Kazal motif (RECK) is a membrane‐anchored glycoprotein that negatively regulates matrix metalloproteinase (MMP) and plays an integral role in cancer invasion and metastasis.…”

Section: Anti‐tumor Mechanismmentioning

confidence: 99%