1,7‐Bis(4‐hydroxyphenyl)‐4‐hepten‐3‐one from <i>Betula platyphylla</i> induces apoptosis by suppressing autophagy flux and activating the p38 pathway in lung cancer cells

Jung, Hyun Jin; Song, Kyung‐Sik; Son, Youn Kyoung; Seong, Je Kyung; Kim, Sun Yeou; Oh, Seung Hyun

doi:10.1002/ptr.6506

Cited by 9 publications

(3 citation statements)

References 31 publications

(32 reference statements)

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“…As previously described, Western blot analysis was performed against anti-Ninj1 (Abclon, Seoul, Korea), anti-pPKCδ/θ (Cell Signaling Technology, MA, USA), anti-actin, and anti-GAPDH (Millipore, Schwalbach, Germany) [52]. Briefly, cell lysates were prepared with modified RIPA buffer containing protease and phosphatase inhibitors, and equivalent amounts of protein were resolved in sodium dodecyl sulfate-polyacrylamide gels.…”

Section: Immunoblottingmentioning

confidence: 99%

Detrimental Role of Nerve Injury-Induced Protein 1 in Myeloid Cells under Intestinal Inflammatory Conditions

Jung

Kang

Pak

et al. 2020

IJMS

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Nerve injury-induced protein 1 (Ninjurin1, Ninj1) is a cell-surface adhesion molecule that regulates cell migration and attachment. This study demonstrates the increase in Ninj1 protein expression during development of intestinal inflammation. Ninj1-deficient mice exhibited significantly attenuated bodyweight loss, shortening of colon length, intestinal inflammation, and lesser pathological lesions than wild-type mice. Although more severe inflammation and serious lesions are observed in wild-type mice than Ninj1-deficient mice, there were no changes in the numbers of infiltrating macrophages in the inflamed tissues obtained from WT and Ninj1-deficient mice. Ninj1 expression results in activation of macrophages, and these activated macrophages secrete more cytokines and chemokines than Ninj1-deficient macrophages. Moreover, mice with conditional deletion of Ninj1 in myeloid cells (Ninj1fl/fl; Lyz-Cre+) alleviated experimental colitis compared with wild-type mice. In summary, we propose that the Ninj1 in myeloid cells play a pivotal function in intestinal inflammatory conditions.

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Section: Immunoblottingmentioning

confidence: 99%

Detrimental Role of Nerve Injury-Induced Protein 1 in Myeloid Cells under Intestinal Inflammatory Conditions

Jung

Kang

Pak

et al. 2020

IJMS

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“…The safety level was measured by evaluating ERK phosphorylation [ 37 ]. Dovitinib (TKI258) is an inhibitor of multiple kinases, including FGFR, VEGFR, and platelet-derived growth factor receptor (PDGFR); its efficacy has been proven in HER2-negative metastatic breast cancer (NCT00958971), and it inhibits the invasion of MDA-MB-231(SA) cells [ 38 , 39 ]. E-3810 inhibits FGFR1 , FGFR2 , CSF1R , VEGFR1 , VEGFR2 , and VEGFR3I [ 40 ].…”

Section: Targets Of Tnbc Under Active Clinical Evaluationmentioning

confidence: 99%

TNBC: Potential Targeting of Multiple Receptors for a Therapeutic Breakthrough, Nanomedicine, and Immunotherapy

Singh

Yadav

2021

Biomedicines

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Triple-negative breast cancer (TNBC) is a heterogeneous, recurring cancer associated with a high rate of metastasis, poor prognosis, and lack of therapeutic targets. Although target-based therapeutic options are approved for other cancers, only limited therapeutic options are available for TNBC. Cell signaling and receptor-specific targets are reportedly effective in patients with TNBC under specific clinical conditions. However, most of these cancers are unresponsive, and there is a requirement for more effective treatment modalities. Further, there is a lack of effective biomarkers that can distinguish TNBC from other BC subtypes. ER, PR, and HER2 help identify TNBC and are widely used to identify patients who are most likely to respond to diverse therapeutic strategies. In this review, we discuss the possible treatment options for TNBC based on its inherent subtype receptors and pathways, such as p53 signaling, AKT signaling, cell cycle regulation, DNA damage, and programmed cell death, which play essential roles at multiple stages of TNBC development. We focus on poly-ADP ribose polymerase 1, androgen receptor, vascular endothelial growth factor receptor, and epidermal growth factor receptor as well as the application of nanomedicine and immunotherapy in TNBC and discuss their potential applications in drug development for TNBC.

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“…PI/RNase staining buffer (0.5 mL) was added, followed by incubation at room temperature and under light for 15 min. Afterward, the cells were stored in ice in the dark and detected using flow cytometry within 1 h (Jung et al, 2020).…”

Section: Flow Cytometric Analysis Of Cell Cyclementioning

confidence: 99%

Ethyl Acetate Extract of Selaginella doederleinii Hieron Induces Cell Autophagic Death and Apoptosis in Colorectal Cancer via PI3K-Akt-mTOR and AMPKα-Signaling Pathways

Wang

et al. 2020

Front. Pharmacol.

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Colorectal cancer is one type of cancer with high incidence rate and high mortality worldwide. Thus, developing new chemotherapeutic drugs is important. The Selaginella doederleinii Hieron ethyl acetate (SDEA) extract showed good anti-colon cancer effect in vitro and in vivo, but its mechanism is unclear. This study aimed to further reveal the anticolon cancer effect of SDEA and its possible mechanism. The effects on cell viability, apoptosis, autophagy, and cell cycle in colorectal cells (HT29 and HCT116) were studied using MTT assay, fluorescence microscopy, transmission electron microscopy, and flow cytometry. The mechanisms were further studied using cell transfection, Western blot, and real-time quantitative polymerase chain reaction assay. The effect of xenotransplantation in vivo was observed using immunohistochemistry. Results showed that SDEA inhibited cell proliferation and induced cell morphological changes, cell cycle arrest, autophagy, and apoptosis. It also induced loss of mitochondrial membrane potential, increased the autophagic flux, raised the ratio of Bax/Bcl-2, activated caspases, and inhibited PI3K-Akt-mTOR signaling pathways. Furthermore, SDEA inhibited the growth of xenograft tumors in a dose-dependent manner. Immunohistochemistry analysis confirmed the alteration of autophagy-and apoptosisrelated proteins and immunohistochemical microvascular density in xenografts, which were consistent with the results in vitro. Therefore, SDEA is important for developing candidate drugs against colorectal cancers.

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1,7‐Bis(4‐hydroxyphenyl)‐4‐hepten‐3‐one from Betula platyphylla induces apoptosis by suppressing autophagy flux and activating the p38 pathway in lung cancer cells

Cited by 9 publications

References 31 publications

Detrimental Role of Nerve Injury-Induced Protein 1 in Myeloid Cells under Intestinal Inflammatory Conditions

Detrimental Role of Nerve Injury-Induced Protein 1 in Myeloid Cells under Intestinal Inflammatory Conditions

TNBC: Potential Targeting of Multiple Receptors for a Therapeutic Breakthrough, Nanomedicine, and Immunotherapy

Ethyl Acetate Extract of Selaginella doederleinii Hieron Induces Cell Autophagic Death and Apoptosis in Colorectal Cancer via PI3K-Akt-mTOR and AMPKα-Signaling Pathways

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