scholarly journals Three New Steroid Biglycosides, Plancisides A, B, and C, from the Starfish Acanthaster planci

2014 ◽  
Vol 9 (9) ◽  
pp. 1934578X1400900 ◽  
Author(s):  
Alla A. Kicha ◽  
Thi H. Dinh ◽  
Natalia V. Ivanchina ◽  
Timofey V. Malyarenko ◽  
Anatoly I. Kalinovsky ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Lines ◽  
Colony Formation ◽  
Clonogenic Assay ◽  
Ethanolic Extract ◽  
Soft Agar ◽  
Steroid Glycoside ◽  
Acanthaster Planci ◽  
Hct 116 ◽  
Soft Agar Clonogenic Assay

Three new steroid biglycosides, plancisides A-C (1-3), were isolated from the ethanolic extract of the starfish Acanthaster planci. The structures of 1-3 were determined by extensive NMR and ESI-MS techniques, as (24 S)-28- O-[β-D-galactofuranosyl-(1→5)-α-L-arabinofuranosyl]-24-methyl-5α-cholestane-3β,4β,6α,8,15β,16β,28-heptol (1), (24 S)-28- O-[α-L-fucopyranosyl-(1→2)-3- O-methyl-β-D-xylopyranosyl]–24-methyl-5α-cholestane-3β,4β,6α,8,15β,16β,28-heptol (2) and (24 S)-28- O-[2,4-di- O-methyl-β-D-xylopyranosyl-(1→2)-α-L-arabinofuranosyl]-24-methyl-5α-cholestane-3β,4β,6α,8,15β,16β,28-heptol 6- O-sulfate (3), respectively. Compound 2 is the first steroid glycoside containing an α-fucopyranose unit found from starfish. Compound 1 slightly inhibits cell proliferation of HCT-116, T-47D, and RPMI-7951 cancer cell lines, but has no effect on colony formation of these cells in a soft agar clonogenic assay.

scholarly journals Two New Asterosaponins from the Far Eastern Starfish Lethasterias fusca

2012 ◽  
Vol 7 (7) ◽  
pp. 1934578X1200700 ◽  
Author(s):  
Natalia V. Ivanchina ◽  
Anatoly I. Kalinovsky ◽  
Alla A. Kicha ◽  
Timofey V. Malyarenko ◽  
Pavel S. Dmitrenok ◽  
...  
Keyword(s):  
Cell Lines ◽  
Clonogenic Assay ◽  
Ethanolic Extract ◽  
Soft Agar ◽  
Chemical Transformations ◽  
Hct 116 ◽  
New Compounds ◽  
Far Eastern ◽  
Soft Agar Clonogenic Assay ◽  
Cell Colony

Two new asterosaponins, lethasteriosides A (1) and B (2), were isolated along with previously known thornasteroside A (3), anasteroside A (4), and luidiaquinoside (5) from the ethanolic extract of the Far Eastern starfish Lethasterias fusca. The structures of the new compounds were elucidated by extensive NMR and ESIMS techniques, and chemical transformations. Compounds 1 and 3–5 did not show any apparent cytotoxicity against cancer cell lines T-47D, RPMI-7951, and HCT-116, but glycoside 1, at concentration of 20 μM, demonstrated considerable inhibition of the T-47D (97%), RPMI-7951 (90%) and HCT-116 (90%) cell colony formations in a soft agar clonogenic assay.

Downregulation of Sulfiredoxin (Srx) Suppressed Cell Proliferation Migration and Invasion Through Inhibiting Extracellular Signal-Regulated Kinase/Nrf2 Pathway in Hepatocellular Carcinoma

2021 ◽  
Vol 11 (11) ◽  
pp. 2137-2145
Author(s):  
Xuejuan Zhu ◽  
Danqian Lu
Keyword(s):  
Cell Proliferation ◽  
Western Blot ◽  
Signaling Pathway ◽  
Cell Lines ◽  
Colony Formation ◽  
Migration And Invasion ◽  
Related Factor ◽  
Extracellular Signal Regulated Kinase ◽  
Extracellular Signal ◽  
Nrf2 Signaling Pathway

Background: Sulfiredoxin (Srx) has been identified to play important roles in the development of various cancers. However, the precise effects and underlying mechanism of Srx on the progression of HCC are far from being fully understood. Materials and Methods: The abundances of Srx in THLE-2 cell and HCC cell lines were determined by western blot and RT-qPCR. Next, SK-Hep-1 cells were transfected with shRNA-Srx or shRNA-NC and treated with TBHQ (an extracellular signal-regulated kinase (ERK) activator) for functional experiments. Then, CCK8 and colony formation assays were used to determine cell proliferation and clone-forming abilities in vitro. Cell migration and invasion were assessed via wound healing and transwell assays. The expression of MMP2, MMP9 and key members in ERK/nuclear factor E2 related factor (Nrf2) signaling pathway was detected by performing western blot analysis. Results: We reported evidence that Srx was frequently up-regulated in HCC cell lines. Srx interference constrained cell proliferation, colony formation rate, migration and invasion of SK-Hep-1 cells. Moreover, mechanistic investigations indicated that Srx interference significantly inhibited the activation of ERK/Nrf2 signaling pathway, and ERK activator TBHQ can reverse the functions of Srx interference in SK-Hep-1 cells. Conclusion: Overall, Downregulation of Srx might impede HCC progression by suppressing ERK/Nrf2 signaling pathway. Findings in the current study reported the functional involvement and molecular mechanism of Srx in HCC, suggesting that Srx might have a potential therapeutic value in HCC treatment.

scholarly journals USP13 Regulates the Breast Tumor Proliferation and Migration through the Stabilization of PDCD4 Protein

2021 ◽  
Author(s):  
Jun Tian ◽  
Bei Li ◽  
Jing Qiao ◽  
Xinfeng Pang ◽  
Xiaojing Yue
Keyword(s):  
Breast Cancer ◽  
Cell Proliferation ◽  
Cell Lines ◽  
Breast Tumor ◽  
Soft Agar ◽  
Tumor Proliferation ◽  
Soft Agar Assay ◽  
And Migration ◽  
Cancer Tissues ◽  
Proliferation And Migration

Abstract Background: Programmed cell death protein 4 (PDCD4), which serves as a tumor suppressor protein, plays a important role in cell proliferation,apoptosis, cell migration and DNA-damage response.However, the exact mechanism for the deubiquitination of PDCD4 remain unclear.Methods: Western blotting was used to detect the expression of PDCD4 in the breast cancer tissues and BC cell lines. We identified the potential PDCD4 associated deubiquitinase by RNAi screening. GST-Pull down and domain-mapping analysis were used to reveal that USP13 and PDCD4 directly interact with each other.Flow cytometry was used to detect the changes of G1 to S phase. Soft agar assay was used to measure the changes of the cell proliferation efficiency.Results: The expression of PDCD4 was decreased in the breast cancer tissues and BC cell lines. USP13 as a potential PDCD4 associated deubiquitinase. USP13 physically interacted with PDCD4 and greatly increased the steady state of PDCD4 through the ubiquitin-proteasome pathway.Importantly, silencing of the USP13 facilitated cell cycle from G1 to Sphase, promoted breast tumor cells proliferation and migration through downregulation of PDCD4. Conclusions: Together, these results suggest that USP13 plays an important role in the breast tumor proliferation and migration through modulating PDCD4 stability.

scholarly journals Hif-1α Inhibitors Could Successfully Inhibit the Progression of Differentiated Thyroid Cancer in Vitro

2020 ◽  
Vol 13 (9) ◽  
pp. 208
Author(s):  
Min-Hee Kim ◽  
Tae Hyeong Lee ◽  
Jin Soo Lee ◽  
Dong-Jun Lim ◽  
Peter Chang-Whan Lee
Keyword(s):  
Cell Proliferation ◽  
Thyroid Cancer ◽  
Cell Lines ◽  
Cancer Progression ◽  
Hypoxia Inducible Factor ◽  
Soft Agar ◽  
Dependent Manner ◽  
Thyroid Cancer Cell Lines ◽  
Dose Dependent

Hypoxia-inducible factor (HIF)-1α plays an important role in cancer progression. In various cancers, including thyroid cancer, overexpression of HIF-1α is related to poor prognosis or treatment response. However, few studies have investigated the role of HIF-1α inhibition in thyroid cancer progression. We evaluated the utility of the HIF-1α inhibitor IDF-11774 in vitro utilizing two thyroid cancer cell lines, K1 and BCPAP. Both cell lines were tested to elucidate the effects of IDF-11774 on cell proliferation and migration using soft agar and invasion assays. Here, we found that a reduction of HIF-1α expression in BCPAP cells was observed after treatment with IDF-11774 in a dose-dependent manner. Moreover, cell proliferation, migration, and anchorage-independent growth were effectively inhibited by IDF-11774 in BCPAP cells but not in K1 cells. Additionally, invasion of BCPAP but not K1 cells was controlled with IDF-11774 in a dose-dependent manner. Our findings suggest that promoting the degradation of HIF-1α could be a strategy to manage progression and that HIF-1α inhibitors are potent drugs for thyroid cancer treatment.

scholarly journals EIF3H promotes aggressiveness of esophageal squamous cell carcinoma by modulating Snail stability

2020 ◽  
Vol 39 (1) ◽  
Author(s):  
Xiaobin Guo ◽  
Rui Zhu ◽  
Aiping Luo ◽  
Honghong Zhou ◽  
Fang Ding ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Squamous Cell Carcinoma ◽  
Esophageal Squamous Cell Carcinoma ◽  
Tumor Growth ◽  
Cell Carcinoma ◽  
Cell Lines ◽  
Squamous Cell ◽  
Colony Formation ◽  
Tumor Growth And Metastasis

Abstract Background Overexpression of eukaryotic translation initiation factor 3H (EIF3H) predicts cancer progression and poor prognosis, but the mechanism underlying EIF3H as an oncogene remains unclear in esophageal squamous cell carcinoma (ESCC). Methods TCGA database and the immunohistochemistry (IHC) staining of ESCC samples were used and determined the upregulation of EIF3H in ESCC. CCK8 assay, colony formation assay and transwell assay were performed to examine the ability of cell proliferation and mobility in KYSE150 and KYSE510 cell lines with EIF3H overexpression or knockdown. Xenograft and tail-vein lung metastatic mouse models of KYSE150 cells with or without EIF3H knockdown were also used to confirm the function of EIF3H on tumor growth and metastasis in vivo. A potential substrate of EIF3H was screened by co-immunoprecipitation assay (co-IP) combined with mass spectrometry in HEK293T cells. Their interaction and co-localization were confirmed using reciprocal co-IP and immunofluorescence staining assay. The function of EIF3H on Snail ubiquitination and stability was demonstrated by the cycloheximide (CHX) pulse-chase assay and ubiquitination assay. The correlation of EIF3H and Snail in clinical ESCC samples was verified by IHC. Results We found that EIF3H is significantly upregulated in esophageal cancer and ectopic expression of EIF3H in ESCC cell lines promotes cell proliferation, colony formation, migration and invasion. Conversely, genetic inhibition of EIF3H represses ESCC tumor growth and metastasis in vitro and in vivo. Moreover, we identified EIF3H as a novel deubiquitinating enzyme of Snail. We demonstrated that EIF3H interacts with and stabilizes Snail through deubiquitination. Therefore, EIF3H could promote Snail-mediated EMT process in ESCC. In clinical ESCC samples, there is also a positive correlation between EIF3H and Snail expression. Conclusions Our study reveals a critical EIF3H-Snail signaling axis in tumor aggressiveness in ESCC and provides EIF3H as a promising biomarker for ESCC treatment.

scholarly journals Aphelasteroside F, a new Asterosaponin from the Far Eastern Starfish Aphelasterias japonica

2016 ◽  
Vol 11 (9) ◽  
pp. 1934578X1601100 ◽  
Author(s):  
Roman S. Popov ◽  
Natalia V. Ivanchina ◽  
Anatoly I. Kalinovsky ◽  
Sofiya D. Kharchenko ◽  
Alla A. Kicha ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Colony Formation ◽  
Carbohydrate Chain ◽  
Ethanolic Extract ◽  
Chemical Transformations ◽  
Aphelasterias Japonica ◽  
New Type ◽  
Toxic Concentrations ◽  
Far Eastern ◽  
Melanoma Cell Lines

A new asterosaponin aphelasteroside F (1) was isolated from the ethanolic extract of the Far Eastern starfish Aphelasterias japonica along with the previously known ophidianoside F (2). The structure of 1 was elucidated by extensive use of NMR and ESI-MS techniques, and chemical transformations. Compound 1 contains a new type of asterosaponin carbohydrate chain linked to C-6 of the steroid aglycone aphelaketotriol. Compounds 1 and 2 at non-toxic concentrations slightly inhibited cell proliferation and colony formation of the cancer melanoma cell lines SK-Mel-28, SK-Mel-5, and RPMI-7951.

Replication Protein A 3 Is Associated with Hepatocellular Carcinoma Tumorigenesis and Poor Patient Survival

2017 ◽  
Vol 36 (1) ◽  
pp. 26-32 ◽  
Author(s):  
Wenbo Xiao ◽  
Jun Zheng ◽  
Baoyong Zhou ◽  
Long Pan
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Tumor Progression ◽  
Colony Formation ◽  
Patient Survival ◽  
Protein A ◽  
Replication Protein A ◽  
Soft Agar ◽  
Replication Protein ◽  
High Expression

Background: Replication protein A (RPA) 3 is a subunit of the RPA protein complex, which functions in multiple processes of DNA metabolism. Dysregulation of RPA1 and RPA2 has been implicated in tumor progression in several cancer types. However, the function of RPA3 in hepatocellular carcinoma (HCC) tumorigenesis has not been elucidated. Method: In this study, we investigated the function of RPA3 in HCC development by stably knocking down its expression using short hairpin RNA (shRNA) in HepG2 cell line, followed by cell proliferation, colony formation, soft agar, and invasion assays. Xenograft experiment was performed to examine in vivo tumor-promoting properties of RPA3. Results: Downregulation of RPA3-inhibited cell proliferation, colony formation, soft agar growth as well as invasion in HepG2 cells were observed. Stable knockdown of RPA3 significantly inhibited tumor growth in the xenograft mouse model. In addition, qRT-PCR analysis revealed that RPA3 was upregulated in human HCC tissues compared with matched noncancerous adjacent tissues (NATs). High expression of RPA3 was associated with poor overall survival and disease-free survival. Conclusion: Elevated expression of RPA3 promotes tumor progression in HCC cells. RPA3 is upregulated in HCC tissues and high expression of RPA3 is associated with poorer patient survival. Therefore, this protein may represent a novel therapeutic target for intervention of HCC and prognostic biomarker for patient survival.

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