Secalonic Acid-D Represses HIF1α/VEGF-Mediated Angiogenesis by Regulating the Akt/mTOR/p70S6K Signaling Cascade

Guru, Santosh Kumar; Pathania, Anup Singh; Kumar, Suresh; Deshidi, Ramesh; Kumar, Manjeet; Rana, Satiander; Kumar, Ajay; Malik, Fayaz; Sharma, Parduman R.; Chandan, B. K.; Jaglan, Sundeep; Sharma, Jai P.; Shah, Bhahwal Ali; Abdullah, Sheikh Tasduq; Lattoo, Surrinder K.; Faruk, Abdul; Saxena, Ajit Kumar; Vishwakarma, Ram A.; Bhushan, Shashi

doi:10.1158/0008-5472.can-14-2312

Cited by 69 publications

(60 citation statements)

References 37 publications

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“…Furthermore, the process of new blood vessels formation (angiogenesis), is another key step in tumor metastasis, which involves several signaling including growth factors and endothelial cell receptors (12). Among them, vascular endothelial growth factor (VEGF), multiple HIF-1α/ VEGF-arbitrated angiogenesis dynamics, by inducing the formation of new blood vessels, was reported by several groups (13)(14)(15) to get an important role in angiogenesis and tumor metastasis.…”

Section: Introductionmentioning

confidence: 99%

Retracted: Forkhead box protein k1 recruits TET1 to act as a tumor suppressor and is associated with MRI detection

Sun

Wang

et al. 2016

Japanese Journal of Clinical Oncology

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Objective: Today, more and more evidence suggests that Foxk proteins (Foxk1 and Foxk2) work as transcriptional repressors in different kinds of cancer, but whether Foxk1 has a role in mediating tumorigenesis in breast cancer, the evidence is rare. Methods: MCF-7 cells transfected with shFoxk1 displayed a mesenchymal morphology and reduced the expression of E-cadherin, and increased the expression of N-cadherin. Transwell invasion assay and living imaging assay show that the overexpression of Foxk1 could inhibit metastasis in vitro and in vivo. Ribonucleic acid sequencing revealed that the knockdown of Foxk1 resulted in the up-regulation of different oncogenes, which was implicated in metastasis and tumor angiopoiesis. Quantitative chromatin immunoprecipitation, chromatin immunoprecipitation and Luciferase reporter assays suggested that Foxk1 could bind to the promoter of epithelial-mesenchymal transition inducer Twist and vascular endothelial growth factor, VEGF. Mass Spectrometry, co-immunoprecipitation assays and glutathione-S-transferase pull-down assay detected that Foxk1 was physically associated with Ten-eleven translocation 1, TET1, in vivo and in vitro. Results: We reported that the mean expression level of Foxk1 in breast cancer was significantly lower than the adjacent noncarcinoma tissue. The higher Foxk1 expression was associated with better prognosis. Endothelial tube formation assays indicated that Foxk1 might regulate breast cancer angiogenesis through transcriptional repression of vascular endothelial growth factor. Furthermore, in vivo magnetic resonance imaging revealed the overexpression of Foxk1 could enhance the detection of the tumors. Further, a strong negative correlation was observed between Foxk1 and Twsit or between Foxk1 and vascular endothelial growth factor, and the higher Foxk1 expression is correlated with better over all survivals and better relapse-free survivals. Conclusions: Together, our data indicated the function of Foxk1 as a tumor suppressor in facilitating angiogenesis and metastasis in breast cancer.

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Section: Introductionmentioning

confidence: 99%

Retracted: Forkhead box protein k1 recruits TET1 to act as a tumor suppressor and is associated with MRI detection

Sun

Wang

et al. 2016

Japanese Journal of Clinical Oncology

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“…It also decreased the percentage of side population cell in lung cancer cells. These results highlight 105 as an interesting molecule that has a potent cytotoxic activity by enduring BCRP degradation, and was considered as a lead compound for the development of new BCRP inhibitors [212]. Chemically, secalonic acid D (105) is the chiral dimeric natural product of ergochrome xanthone [213].…”

Section: Secalonic Acid Dmentioning

confidence: 99%

Marine Natural Products as Models to Circumvent Multidrug Resistance

et al. 2016

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Multidrug resistance (MDR) to anticancer drugs is a serious health problem that in many cases leads to cancer treatment failure. The ATP binding cassette (ABC) transporter P-glycoprotein (P-gp), which leads to premature efflux of drugs from cancer cells, is often responsible for MDR. On the other hand, a strategy to search for modulators from natural products to overcome MDR had been in place during the last decades. However, Nature limits the amount of some natural products, which has led to the development of synthetic strategies to increase their availability. This review summarizes the research findings on marine natural products and derivatives, mainly alkaloids, polyoxygenated sterols, polyketides, terpenoids, diketopiperazines, and peptides, with P-gp inhibitory activity highlighting the established structure-activity relationships. The synthetic pathways for the total synthesis of the most promising members and analogs are also presented. It is expected that the data gathered during the last decades concerning their synthesis and MDR-inhibiting activities will help medicinal chemists develop potential drug candidates using marine natural products as models which can deliver new ABC transporter inhibitor scaffolds.

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“…15 All the experiments were performed in triplicate. 14 Briefly, the cells were seeded in 6-well plates at a density of 5 × 10 3 cells per well, transfected with siRNA after 24 hours of incubation at 37°C and 5% CO 2 in a humidified incubator, and grown for over 12 days.…”

Section: Cell Proliferation Assaymentioning

confidence: 99%

MARCH1 encourages tumour progression of hepatocellular carcinoma via regulation of PI3K‐AKT‐β‐catenin pathways

Xie

Dai

et al. 2019

J Cellular Molecular Medi

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Membrane‐associated RING‐CH‐1 (MARCH1) is a membrane‐anchored E3 ubiquitin ligase that is involved in a variety of cellular processes. MARCH1 was aberrantly expressed as a tumour promoter in ovarian cancer, but the signalling about the molecular mechanism has not yet been fully illuminated. Here, we first determined that MARCH1 was obviously highly expressed in human hepatocellular carcinoma samples and cells. In addition, our findings demonstrated that the proliferation, migration and invasion of hepatocellular carcinoma were suppressed, but the apoptosis was increased, as a result of MARCH1 knockdown by either siRNA targeting MARCH1 or pirarubicin treatment. Conversely, the proliferation, migration and invasion of hepatocellular carcinoma were obviously accelerated, and the apoptosis was decreased, by transfecting the MARCH1 plasmid to make MARCH1 overexpressed. Moreover, in vivo, the results exhibited a significant inhibition of the growth of hepatocellular carcinoma in nude mice, which were given an intra‐tumour injection of siRNA targeting MARCH1. Furthermore, our study concluded that MARCH1 functions as a tumour promoter, and its role was up‐regulated the PI3K‐AKT‐β‐catenin pathways both in vitro and in vivo. In summary, our work determined that MARCH1 has an important role in the development and progression of hepatocellular carcinoma and may be used as a novel potential molecular therapeutic target in the future treatment of hepatocellular carcinoma.

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Secalonic Acid-D Represses HIF1α/VEGF-Mediated Angiogenesis by Regulating the Akt/mTOR/p70S6K Signaling Cascade

Cited by 69 publications

References 37 publications

Retracted: Forkhead box protein k1 recruits TET1 to act as a tumor suppressor and is associated with MRI detection

Retracted: Forkhead box protein k1 recruits TET1 to act as a tumor suppressor and is associated with MRI detection

Marine Natural Products as Models to Circumvent Multidrug Resistance

MARCH1 encourages tumour progression of hepatocellular carcinoma via regulation of PI3K‐AKT‐β‐catenin pathways

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