Baicalin inhibits human osteosarcoma cells invasion, metastasis, and anoikis resistance by suppressing the transforming growth factor-β1-induced epithelial-to-mesenchymal transition

Wang, Yanmao; Wang, Huimin; Zhou, Runhua; Zhong, Wanrun; Lu, Shengdi; Chai, Yimin

doi:10.1097/cad.0000000000000495

Cited by 36 publications

(23 citation statements)

References 30 publications

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“…Among several potentiating factors of metastasis, the transition of epithelial to mesenchymal phenotype, known as EMT [ 6 , 37 , 38 ], has garnered most attention [ 39 – 41 ]. EMT has been shown to facilitate cancer progression and aggressive behaviors of cancer cells, such as increased cell migration and invasion, and anoikis resistance [ 42 – 46 ]. Here, we found that phoyunnanin E, a pure compound isolated from D. venustum and related species, has anti-migration and EMT-suppression activities.…”

Section: Discussionmentioning

confidence: 99%

Phoyunnanin E inhibits migration of non-small cell lung cancer cells via suppression of epithelial-to-mesenchymal transition and integrin αv and integrin β3

Petpiroon

Sritularak

Chanvorachote

2017

BMC Complement Altern Med

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BackgroundThe conversion of the epithelial phenotype of cancer cells into cells with a mesenchymal phenotype-so-called epithelial–mesenchymal transition (EMT)-has been shown to enhance the capacity of the cells to disseminate throughout the body. EMT is therefore becoming a potential target for anti-cancer drug discovery. Here, we showed that phoyunnanin E, a compound isolated from Dendrobium venustum, possesses anti-migration activity and addressed its mechanism of action.MethodsThe cytotoxic and proliferative effects of phoyunnanin E on human non-small cell lung cancer-derived H460, H292, and A549 cells and human keratinocyte HaCaT cells were investigated by MTT assay. The effect of phoyunnanin E on EMT was evaluated by determining the colony formation and EMT markers. The migration and invasion of H460, H292, A549 and HaCaT cells was evaluated by wound healing assay and transwell invasion assay, respectively. EMT markers, integrins and migration-associated proteins were examined by western blot analysis.ResultsPhoyunnanin E at the concentrations of 5 and 10 μM, which are non-toxic to H460, H292, A549 and HaCaT cells showed good potential to inhibit the migratory activity of three types of human lung cancer cells. The anti-migration effect of phoyunnanin E was shown to relate to the suppressed EMT phenotypes, including growth in anchorage-independent condition, cell motility, and EMT-specific protein markers (N-cadherin, vimentin, slug, and snail). In addition to EMT suppression, we found that phoyunnanin E treatment with 5 and 10 μM could decrease the cellular level of integrin αv and integrin β3, these integrins are frequently up-regulated in highly metastatic tumor cells. We further characterized the regulatory proteins in cell migration and found that the cells treated with phoyunnanin E exhibited a significantly lower level of phosphorylated focal adhesion kinase (p-FAK) and phosphorylated ATP-dependent tyrosine kinase (p-AKT), and their downstream effectors (including Ras-related C3 botulinum (Rac-GTP); Cell division cycle 42 (Cdc42); and Ras homolog gene family, member A (Rho-GTP)) in comparison to those of the non-treated control.ConclusionsWe have determined for the first time that phoyunnanin E could inhibit the motility of lung cancer cells via the suppression of EMT and metastasis-related integrins. This new information could support further development of this compound for anti-metastasis approaches.

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Section: Discussionmentioning

confidence: 99%

Phoyunnanin E inhibits migration of non-small cell lung cancer cells via suppression of epithelial-to-mesenchymal transition and integrin αv and integrin β3

Petpiroon

Sritularak

Chanvorachote

2017

BMC Complement Altern Med

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“…Moreover, SOX18 silencing increased E‐cadherin and decreased Vimentin and β‐catenin expression in OS cells, while SOX18 overexpression decreased E‐cadherin and increased Vimentin and β‐catenin expression. Increased E‐cadherin and decreased vimentin expression inhibited U2OS cells invasion and migration . Increased β‐catenin and decreased E‐cadherin expression was also found to be linked to an increased metastasizing ability of the tumor and worse prognosis for the osteosarcoma patients …”

Section: Discussionmentioning

confidence: 93%

Heterogeneous expression and biological function of SOX18 in osteosaroma

Zhu

Yang

et al. 2018

J of Cellular Biochemistry

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Osteosaroma (OS) is a primary bone malignancy and is associated with high morbidity. Sex determining region Y-box 18 (SOX18) is identified overexpressed in OS. However, the molecular mechanism underlying the biological function of SOX18 in OS is still unclear. The aim of the current study was to determine the SOX18 expression in patients with OS and its effect on tumor cell malignant phenotypes. Our results showed that SOX18 was overexpressed in OS patients from both E-MEXP-3628 database and independent samples from our hospital and in OS cell lines. SOX18 silencing significantly induced G0-G1 phase cell cycle arrest and apoptosis and inhibited U-2OS cell migration and invasion and cell growth both in vitro and in vivo. However, SOX18 overexpression remarkably promoted 143B cell proliferation, migration and invasion and inhibited cell cycle arrest and apoptosis. The protein expression levels of p53, p21, Bax, Bcl-2, and Caspase-3 were also regulated by SOX18. Moreover, SOX18 was found negative correlated with the expression of HERC1, HER2, HERC3, HERC4, HERC5, and HERC6 in OS patients and in OS cells, with the most significant correlation detected in HERC2 expression, which was following found interacted with SOX18 in OS cells. Taken together, our results suggest that SOX18 is overexpressed in OS and plays an important role in proliferation, apoptosis, migration and invasion of OS cells, and may provide a novel and promising thera-peutic strategy for OS.

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“…As a tumor prone to spread from the initially affected bone to more sites, it is notable that osteosarcoma is also accompanied by signi cant EMT changes. Inhibiting the EMT of osteosarcoma cells can not only suppress the development of metastasis, but also decrease the resistance to osteosarcoma chemotherapy [45][46]. Twist1, belonging to the bHLH (basic helix loop helix) transcription factor family, has been con rmed by mounting studies that it can regulate the EMT of tumor cells.…”

Section: Discussionmentioning

confidence: 99%

Down-regulating lncRNA LINC00485 inhibits the development of osteosarcoma by regulating miR-361-5p/Twist1 axis

Hu¹,

Luo²,

Zhou³

et al. 2020

Preprint

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Background: Mounting researches have established that long-chain non-coding RNA (lncRNA) and microRNA (miRNA) occupy an essential position in osteosarcoma development. The present study attempted to explicate the functional role and mechanism of LINC00485 and miR-361-5p in regulating the osteosarcoma progression.Methods: RT-PCR was employed to measure LINC00485 expression in osteosarcoma tissues and adjacent healthy tissues. Moreover, the correlation between LINC00485 expression and the clinicopathological indexes was analyzed. Further, the LINC00485 low-expressed cell model was constructed, and the CCK8 assay was employed to measure cell proliferation, followed by the flow cytometry in apoptosis testing. Besides, Transwell assay was utilized to detect cell migration and invasion ability, and Western blot examined the alternations of epithelial mesenchymal transition (EMT) marker molecules (E-cadherin and Vimentin). Furthermore, bioinformatics analysis was taken advantage of predicting the downstream molecular targets of LINC00485. RT-PCR and Western blot were carried out respectively to estimate the expression variations of miR-361-5p and Twist1. Dual luciferase activity assay and RNA co-precipitation (RIP) assay were conducted to verify the targeting relationship between LINC00485 and miR-361-5p, miR-361-5p and Twist1.Results: In comparison with normal adjacent tissues, the LINC00485 expression in cancer tissues was profoundly up-regulated. LINC00485 low expression greatly attenuated proliferation, migration, invasion, and EMT in osteosarcoma cells, while enhancing apoptosis. Bioinformatics analysis claimed that miR-361-5p was a sponge miRNA for LINC00485, targeting the Twist1 expression. Further gain- and loss-experiments declared that miR-361-5p limited the osteosarcoma development by inhibiting osteosarcoma cell proliferation, metastasis and promoting apoptosis.Conclusions: LINC00485 acted as an oncogene in the osteosarcoma tumorigenesis by modulating the miR-361-5p/Twist1 axis.

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Baicalin inhibits human osteosarcoma cells invasion, metastasis, and anoikis resistance by suppressing the transforming growth factor-β1-induced epithelial-to-mesenchymal transition

Cited by 36 publications

References 30 publications

Phoyunnanin E inhibits migration of non-small cell lung cancer cells via suppression of epithelial-to-mesenchymal transition and integrin αv and integrin β3

Phoyunnanin E inhibits migration of non-small cell lung cancer cells via suppression of epithelial-to-mesenchymal transition and integrin αv and integrin β3

Heterogeneous expression and biological function of SOX18 in osteosaroma

Down-regulating lncRNA LINC00485 inhibits the development of osteosarcoma by regulating miR-361-5p/Twist1 axis

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