TPGS-modified liposomes for the delivery of ginsenoside compound K against non-small cell lung cancer: formulation design and its evaluation <i>in vitro</i> and <i>in vivo</i>

Yang, Lei; Jin, Xin; Zhang, Zhenhai; Yan, Hongmei; Wang, Jing; Sun, E; Hou, Jian; Jia, Xiao‐Bin; Lv, Huixia

doi:10.1111/jphp.12590

Cited by 59 publications

(51 citation statements)

References 34 publications

(51 reference statements)

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“…C-K is the major metabolite of ginsenoside and has been shown to possess effective anti-cancer capabilities in a variety of tumors, including NSCLC (Yang et al 2016).…”

Section: Discussionmentioning

confidence: 99%

“…Compound K (C-K, 20-O-(β-D-glucopyranosyl)-20(S)-protopanaxadiol) is the main metabolite product of ginsenoside, and has been found to inhibit the proliferation in a variety of cancers (Lee et al 1999;Zhou et al 2006). The delivery and efficiency of C-K mixed with micelles was significantly improved, which enhanced the antitumour efficacy of C-K in lung cancer (Yang et al 2016;Zhang et al 2017). In addition, C-K combination with gamma-ray radiation or cisplatin enhanced the efficacy of radiotherapy and chemotherapy in lung cancer (Chae et al 2009;Li et al 2015).…”

Section: Introductionmentioning

confidence: 99%

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Ginsenoside metabolite compound K induces apoptosis and autophagy in non-small cell lung cancer cells via AMPK–mTOR and JNK pathways

Dong

Wang

et al. 2019

Biochem. Cell Biol.

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Compound K [C-K; 20-O-(β-d-glucopyranosyl)-20(S)-protopanaxadiol], as a metabolite of ginsenoside, has been verified to have antitumor effects in various cancers, including non-small cell lung cancer (NSCLC). However, the detailed mechanisms of C-K in NSCLC remain largely unknown. In this study, we aimed to evaluate the effect of C-K on apoptosis and autophagy in NSCLC cells as well as its related mechanisms. According to the results, C-K suppressed the proliferation, and led to G1 phase arrest and apoptosis in A549 and H1975 cells. Subsequently, C-K promoted autophagy, as confirmed by the enhanced rate of cells staining positive with acridine orange, increased levels of LC3II and Beclin-1, and with decreased levels of p62 in A549 and H1975 cells. Moreover, 3-methyladenine (3-MA; an inhibitor of autophagy) effectively suppressed the inhibition of proliferation and apoptosis that was induced with C-K. Finally, C-K treatment promoted the activation of the AMPK–mTOR and c-Jun N-terminal kinase (JNK) signaling pathways. Treatment with compound C (AMPK inhibitor) or SP600125 (JNK inhibitor) significantly restrained the inhibition of proliferation, apoptosis, and autophagy induced with C-K in A549 and H1975 cells. In conclusion, this study demonstrates that C-K promotes autophagy-mediated apoptosis in NSCLC via AMPK–mTOR and JNK signaling pathways.

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“…C-K is the major metabolite of ginsenoside and has been shown to possess effective anti-cancer capabilities in a variety of tumors, including NSCLC (Yang et al 2016).…”

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Ginsenoside metabolite compound K induces apoptosis and autophagy in non-small cell lung cancer cells via AMPK–mTOR and JNK pathways

Dong

Wang

et al. 2019

Biochem. Cell Biol.

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“…Studies have confirmed that CK has an inhibitory effect on various tumor cells, including liver, lung, breast and colon cancer as well as leukemia (12,(17)(18)(19). The antitumor effect of CK is mainly reflected in its ability to significantly attenuate the proliferation, invasion, and migration of tumor cells.…”

Section: Discussionmentioning

confidence: 98%

Ginsenoside CK induces apoptosis and suppresses proliferation and invasion of human osteosarcoma cells through the PI3K/mTOR/p70S6K1 pathway

et al. 2020

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Osteosarcoma is one of the most malignant bone tumors, and its major threats are aggressive invasion and early tumor metastasis, which result in a poor prognosis and high mortality. Accumulating evidence indicates that ginsenoside compound K (CK) has a significant antitumor effect, particularly on the inhibition of proliferation and invasion of numerous human tumors. In the present study, it was revealed that CK inhibited the viability and proliferation of osteosarcoma cells. Moreover, it was demonstrated that CK induced apoptosis and inhibited the migration and invasion of osteosarcoma cells via apoptotic staining, Annexin V/PI staining, and Transwell invasion assays. Furthermore, at the molecular level, the present results confirmed that apoptosis and invasion-related proteins were regulated by CK, which was possibly related to the blockade of the PI3K/mTOR/p70S6K1 signaling pathway. In summary, the present findings indicated that CK inhibited viability and proliferation, induced apoptosis, and inhibited the migration and invasion of osteosarcoma cells through the PI3K/mTOR/p70S6K1 signaling pathway.

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“…The concentration of NCTD encapsulated by the micelles with core-shell structure was measured using high-performance liquid chromatography at 254 nm (HPLC; Agilent LC1260, USA). In brief, NCTD-M was diluted five times with methanol (chromatographic grade) and filtered with a 0.45 lm microporous membrane [22]. Drug loading (DL %) and encapsulation efficiency (EE %) were calculated using the following equations:…”

Section: Drug Content and Entrapment Efficiencymentioning

confidence: 99%

Promising positive liver targeting delivery system based on arabinogalactan-anchored polymeric micelles of norcantharidin

Zhang

Yang

Hou

et al. 2018

Artificial Cells, Nanomedicine, and Biotechnology

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2018) Promising positive liver targeting delivery system based on arabinogalactananchored polymeric micelles of norcantharidin, Artificial Cells, Nanomedicine, and Biotechnology, 46:sup3, S630-S640, ABSTRACT Liver cancer is the third most common cause of global cancer-related deaths. This study focused on newly developed drug delivery systems with hepatocyte asialoglycoprotein receptor binding targeting the liver. Although norcantharidin (NCTD) is effective in primary liver cancer treatment, its toxicity in the urinary system remains. Positive liver-targeting effect could be achieved by preparing polymer micelles by arabinogalactan on the surface of N-(4-methylimidazole)-hydroxyethyl-chitosan (MHC).HepG2 cells were used to analyze the cytotoxicity, invasion, apoptosis and uptake of NCTD-loaded micelles. The in vivo antitumor efficacy of NCTD-M was evaluated using tumor-bearing nude mice. Successful preparation of NCTD-M was shown. In vivo imaging showed that micelles significantly increased positive liver drug targeting. Laser confocal microscopy showed increased cellular uptake of micelles. NCTD-M also enhanced cell invasion and the proportion of apoptotic cells. Compared with the other groups, the micelles showed better antitumor effects in vivo. Therefore, the positive liver-targeting NCTD-M, which can enhance antitumor efficacy and reduce toxicity, could be a promising and effective therapeutic agent for liver cancer treatment.

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TPGS-modified liposomes for the delivery of ginsenoside compound K against non-small cell lung cancer: formulation design and its evaluation in vitro and in vivo

Abstract: The novel GCKT-liposomes significantly improved the antitumour efficacy of GCK.

Cited by 59 publications

References 34 publications

Ginsenoside metabolite compound K induces apoptosis and autophagy in non-small cell lung cancer cells via AMPK–mTOR and JNK pathways

Ginsenoside metabolite compound K induces apoptosis and autophagy in non-small cell lung cancer cells via AMPK–mTOR and JNK pathways

Ginsenoside CK induces apoptosis and suppresses proliferation and invasion of human osteosarcoma cells through the PI3K/mTOR/p70S6K1 pathway

Promising positive liver targeting delivery system based on arabinogalactan-anchored polymeric micelles of norcantharidin

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