Casticin inhibits self-renewal of liver cancer stem cells from the MHCC97 cell line

He, Guicheng; Cao, Xiaocheng; He, Meng; Sheng, Xin; Wu, Yuehua; Ai, Xiaohong

doi:10.3892/ol.2014.1972

Cited by 27 publications

(16 citation statements)

References 26 publications

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“…He et al (22) found that casticin inhibited epithelialmesenchymal transition (EMT) in liver cancer stem cells from the SMMC-7721 cell line by downregulating Twist. He et al (23) demonstrated casticin also suppressed self-renewal ability in liver cancer stem cells from the MHCC97 cell line. Our previous study showed that casticin suppressed the self-renewal and invasion abilities of LCSLCs from NSCLC A549 cells through p-Akt downregulation (17).…”

Section: Discussionmentioning

confidence: 99%

Casticin suppresses the carcinogenesis of small cell lung cancer H446 cells through activation of AMPK/FoxO3a signaling

Gong

Cao

et al. 2018

Oncol Rep

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Casticin, a natural polymethoxyflavone isolated from A. annua, V. trifolia, and V. agnus‑castus induces apoptosis in cancer cells by activating FoxO3a. However, whether casticin inhibits in vitro carcinogenesis and cancer stem cell (CSC) characteristics, and whether casticin activates FoxO3a in small cell lung cancer (SCLC) cells remain unclear. We here demonstrated that casticin decreased sphere‑ and colony‑formation capabilities, and downregulated uPAR and CD133 in second‑generation spheres, which were considered as lung cancer stem‑like cells (LCSLCs), from SCLC H446 cells, in a concentration‑dependent manner. In addition, casticin dose‑dependently elevated the phosphorylation levels of AMPK and ACC, and reduced p‑FoxO3a expression. The above effects were attenuated by AMPK knockdown with small interfering RNAs (siRNAs). FoxO3a silencing resulted in decreased protein expression of FoxO3a, increased in vitro carcinogenesis and CSC characteristics, with no appreciable effects on AMPK and ACC phosphorylation, and displayed similar activities to those neutralizing the effects of casticin on in vitro carcinogenesis and CSC characteristics. These findings reveal a novel mechanism for regulating AMPK/FoxO3a signaling in response to casticin, suggesting a new strategy for SCLC therapy by targeting cancer stem‑like cells.

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Section: Discussionmentioning

confidence: 99%

Casticin suppresses the carcinogenesis of small cell lung cancer H446 cells through activation of AMPK/FoxO3a signaling

Gong

Cao

et al. 2018

Oncol Rep

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“…Casticin, an anti-inflammatory molecule (32), inhibits numerous cancer cells (27,28,33). Previous studies demonstrated that casticin inhibited EMT in liver cancer stem cells (28) and induced apoptosis in ovarian cancer cells (29).…”

Section: Discussionmentioning

confidence: 99%

“…Casticin, a biologically active component of Fructus viticis (20), possesses numerous biological and pharmacological effects, including immunomodulatory, anti-hyperprolactinemia, neuroprotective and anti-inflammatory properties (22)(23)(24)(25), and alters tumorigenesis and tumor progression (26,27). Additionally, it has been demonstrated that casticin suppresses EMT in hepatocellular carcinoma (28).…”

Section: Introductionmentioning

confidence: 99%

Casticin inhibits the epithelial-mesenchymal transition in ovarian carcinoma via the hedgehog signaling pathway

et al. 2018

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Abstract. Casticin inhibits migration, invasion and induced apoptosis in numerous cancer cells; however, the Hedgehog (Hh) signaling pathway is a key factor in the epithelial-mesenchymal transition (EMT). The present study aimed to assess whether casticin affects the expression of members of the Hh signaling pathway and EMT effectors in ovarian carcinoma. The ovarian cancer SKOV3 cell line was incubated in the presence of various concentrations of casticin or cyclopamine. Next, the expression levels of the main Hh signaling effector glioma-associated oncogene-1 (Gli-1) and EMT-associated factors [Twist-related protein 1 (Twist1), E-cadherin and N-cadherin] were determined by western blotting and reverse transcription-quantitative polymerase chain reaction. Cell proliferation and growth were assessed using MTT and soft agar assays; cell migration and invasion was evaluated using an in vitro migration assay and a transwell invasion assay, respectively. Compared with control group values, Gli-1, Twist1 and N-cadherin expression levels were reduced, whereas E-cadherin levels were increased in the casticin-and cyclopamine-treated groups. Incubation with casticin or cyclopamine resulted in markedly reduced SKOV3 cell viability, migration and invasion, in a dose-dependent manner. To the best of our knowledge, the findings of the present study indicated for first time that casticin may inhibit EMT via Hh signaling in vitro, reducing the migratory ability of ovarian cancer cells.

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“…Many studies have been carried out on the effect of casticin on liver cancer stem cells (LCSCs) derived from the HCC cell cline. One such study conducted on the MHCC97 cell line found that casticin (IC50 value: 17.9 µM and 0.5 µM for parental cells and LCSCs, respectively) inhibited proliferative properties in a dose-dependent matter through the downregulation of B-catenin and blocking the Wnt/β-catenin pathway; the pathway regulates stem cell self-renewal and is present in liver cancer [76]. Another study evidenced the ability of casticin to induce apoptosis and G2/M cell cycle arrest in HepG2 and PLC/PRF/5 cells.…”

Section: Casticin and Hepatocellular Carcinomamentioning

confidence: 99%

An Overview of the Potential Antineoplastic Effects of Casticin

et al. 2020

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Cancer persists as one of the leading causes of deaths worldwide, contributing to approximately 9.6 million deaths per annum in recent years. Despite the numerous advancements in cancer treatment, there is still abundant scope to mitigate recurrence, adverse side effects and toxicities caused by existing pharmaceutical drugs. To achieve this, many phytochemicals from plants and natural products have been tested against cancer cell lines in vivo and in vitro. Likewise, casticin, a flavonoid extracted from the Vitex species, has been isolated from the leaves and seeds of V. trifolia and V. agnus-castus. Casticin possesses a wide range of therapeutic properties, including analgesic, anti-inflammatory, antiangiogenic, antiasthmatic and antineoplastic activities. Several studies have been conducted on the anticancer effects of casticin against cancers, including breast, bladder, oral, lung, leukemia and hepatocellular carcinomas. The compound inhibits invasion, migration and proliferation and induces apoptosis (casticin-induced, ROS-mediated and mitochondrial-dependent) and cell cycle arrest (G0/G1, G2/M, etc.) through different signaling pathways, namely the PI3K/Akt, NF-κB, STAT3 and FOXO3a/FoxM1 pathways. This review summarizes the chemo-preventive ability of casticin as an antineoplastic agent against several malignancies.

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Casticin inhibits self-renewal of liver cancer stem cells from the MHCC97 cell line

Cited by 27 publications

References 26 publications

Casticin suppresses the carcinogenesis of small cell lung cancer H446 cells through activation of AMPK/FoxO3a signaling

Casticin suppresses the carcinogenesis of small cell lung cancer H446 cells through activation of AMPK/FoxO3a signaling

Casticin inhibits the epithelial-mesenchymal transition in ovarian carcinoma via the hedgehog signaling pathway

An Overview of the Potential Antineoplastic Effects of Casticin

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