2-O-Methylmagnolol upregulates the long non-coding RNA, GAS5, and enhances apoptosis in skin cancer cells

Wang, Tong Hong; Chan, Chieh-Wen; Fang, Jia‐You; Shih, Ya-Min; Liu, Yiwen; Wang, Tzu-Chien V.; Chen, Chi-Yuan

doi:10.1038/cddis.2017.66

Cited by 44 publications

(37 citation statements)

References 40 publications

(54 reference statements)

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“…The increased antitumor activity of MM1 has been shown to correlate with its increased ability to induce apoptosis in skin cancer cells [17]. In the same study, we have presented preliminary data to indicate that such a mechanism also apply to oral cancer cells SAS.…”

Section: Effects Of Magnolol and Mm1 On Apoptosis And Il6-stat3 Pathwsupporting

confidence: 48%

“…It has been suggested that the improved antitumor activity of MM1 in skin cancer cells may attribute to the upregulation of lncRNA GAS5 and the enhancement of apoptosis [17]. While we have observed that MM1 displays a greater ability than magnolol to induce apoptosis in OSCC cells (Fig.…”

Section: Effects Of Magnolol and Mm1 On Apoptosis And Il6-stat3 Pathwcontrasting

confidence: 38%

“…While both MM1 and M2M exhibited improved antiinflammatory activity [16], only MM1 displayed an increased anti-tumor activity against skin cancer cells than magnolol both in vitro and in vivo [17]. This finding suggests that MM1 may also display improved anti-tumor activity against other types of cancers, and therefore may be further explored as a potential therapeutic agent for many different cancers.…”

Section: Introductionmentioning

confidence: 72%

“…Assays for viability (by staining with trypane blue), and clonogenic ability were performed as described previously [17,19]. …”

Section: Assays For Cell Proliferation and Clonogenic Abilitymentioning

confidence: 99%

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2-O-Methylmagnolol Induces Apoptosis and Inhibits IL-6/STAT3 Signaling in Oral Squamous Cell Carcinoma

Wang

Fang

et al. 2018

Cell Physiol Biochem

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Background/Aims: 2-O-methylmagnolol (MM1), a derivative of magnolol bearing one methoxy moiety, has been shown to display improved anti-tumor activity against skin cancers. In this study, we examined the anti-tumor effects of magnolol and MM1 on oral squamous cell carcinoma (OSCC). Methods: Trypane blue staining and clonogenic assays were performed to determine the cytotoxic effects of magnolol and MM1 in OSCC cells. Migration and matrigel invasion assays were carried out to examine the metastasis effects of magnolol and MM1 in OSCC cells. IL6-stimulation, Western blot, and immunohistochemistry were used to investigate the IL-6/STAT3 signaling and apoptosis. A bioluminescent mouse model of orthotopically implanted SAS cells was used to determine the anti-tumor activity of MM1 in vivo. Results: MM1 displays greater activity than magnolol on affecting the cytotoxicity, migration, and invasion of OSCC cells cultured in vitro. The improved anti-tumor activity of MM1 was shown to associate with its greater activity to inhibit STAT3 signaling and to induce apoptosis in the OSCC. In addition, we presented evidence that MM1 is effective in inhibiting the growth of orthotopic implanted OSCC cells in vivo. Conclusion: Our data indicate that MM1 displays greater anti-tumor activity than magnolol in OSCC and is an attractive agent to be further explored for its potential clinical application.

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Section: Effects Of Magnolol and Mm1 On Apoptosis And Il6-stat3 Pathwsupporting

confidence: 48%

Section: Effects Of Magnolol and Mm1 On Apoptosis And Il6-stat3 Pathwcontrasting

confidence: 38%

Section: Introductionmentioning

confidence: 72%

“…Assays for viability (by staining with trypane blue), and clonogenic ability were performed as described previously [17,19]. …”

Section: Assays For Cell Proliferation and Clonogenic Abilitymentioning

confidence: 99%

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2-O-Methylmagnolol Induces Apoptosis and Inhibits IL-6/STAT3 Signaling in Oral Squamous Cell Carcinoma

Wang

Fang

et al. 2018

Cell Physiol Biochem

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“…Zhou et al demonstrated that downregulation of lncRNA MEG3 mediated by DNMT3b contributed to nickel malignant transformation of human bronchial epithelial cells via modulating PHLPP1 transcription and HIF-1α translation (11). Wang et al uncovered that 2-O-Methylmagnolol upregulated the long non-coding RNA, GAS5, and enhanced apoptosis in skin cancer cells (12). Several other studies also demonstrated the function of lncRNAs in BC (13)(14)(15).…”

Section: Introductionmentioning

confidence: 95%

lncRNA SNHG5 is associated with poor prognosis of bladder cancer and promotes bladder cancer cell proliferation through targeting p27

Xue

et al. 2017

Oncol Lett

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Abstract. Long non-coding RNAs (lncRNAs) have been identified as critical regulators in tumorigenesis. In our present study, we measured the level of small nucleolar RNA host gene 5 (SNHG5) in bladder cancer (BC) tissues and cell lines, and the correlation of the level of SNHG5 with clinicopathological features and prognosis of BC patients was analyzed. Reverse transcription-quantitative polymerase chain reaction was performed to determine the level of SNHG5 in the BC tissues and cell lines. The Kaplan-Meier method was used to analyze the long-term survival outcomes. MTT and colony formation assays were applied to assess the influence of SNHG5 on cell proliferation ability. Flow cytometry was used to measure the function of SNHG5 on cell cycle and apoptosis rate. SNGH5 was found upregulated in BC tissues and cell lines and a high level of SNGH5 was correlated with a poor prognosis. Silencing SNHG5 inhibited the proliferation ability of BC cells and such a function was attributed to its influence on cells cycle and apoptosis. Our findings imply that SNHG5 was upregulated in BC tissues and played an important role in BC progression and may be a potential therapeutic target for BC patients.

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Magnolol induces cell death through PI3K/Akt‐mediated epigenetic modifications boosting treatment of BRAF‐ and NRAS‐mutant melanoma

et al. 2019

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Most BRAF‐mutant melanoma patients experience a fulminate relapse after several months of treatment with BRAF/MEK inhibitors. To improve therapeutic efficacy, natural plant‐derived compounds might be considered as potent additives. Here, we show that magnolol, a constituent of Magnolia officinalis, induced G1 arrest, apoptosis and cell death in BRAF‐ and NRAS‐mutant melanoma cells at low concentration, with no effect in BRAF‐ and NRAS wild‐type melanoma cells and human keratinocytes. This was confirmed in a 3D spheroid model. The apoptosis‐inducing effect of magnolol was completely rescued by activating Akt suggesting a mechanism relying primarily on Akt signaling. Magnolol significantly downregulated the PI3K/Akt pathway which led to a global decrease of the active histone mark H3K4me3. Alongside, the repressive histone mark H3K9me3 was increased as a response to DNA damage. Magnolol‐induced alterations of histone modifications are reversible upon activation of the Akt pathway. Magnolol‐induced a synergistic effect in combination with either BRAF/MEK inhibitors dabrafenib/trametinib or docetaxel at a lower concentration than usually applied in melanoma patients. Combination of magnolol with targeted therapy or chemotherapy also led to analogous effects on histone marks, which was rescued by Akt pathway activation. Our study revealed a novel epigenetic mechanism of magnolol‐induced cell death in melanoma. Magnolol might therefore be a clinically useful addition to BRAF/MEK inhibitors with enhanced efficacy delaying or preventing disease recurrence.

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2-O-Methylmagnolol upregulates the long non-coding RNA, GAS5, and enhances apoptosis in skin cancer cells

Cited by 44 publications

References 40 publications

2-O-Methylmagnolol Induces Apoptosis and Inhibits IL-6/STAT3 Signaling in Oral Squamous Cell Carcinoma

2-O-Methylmagnolol Induces Apoptosis and Inhibits IL-6/STAT3 Signaling in Oral Squamous Cell Carcinoma

lncRNA SNHG5 is associated with poor prognosis of bladder cancer and promotes bladder cancer cell proliferation through targeting p27

Magnolol induces cell death through PI3K/Akt‐mediated epigenetic modifications boosting treatment of BRAF‐ and NRAS‐mutant melanoma

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