Honokiol Inhibits Melanoma Growth by Targeting Keratin 18 in vitro and in vivo

Liu, Tingting; Liu, Hui; Wang, Penglei; Hu, Yamei; Yang, Ran; Liu, Fangfang; Kim, Hong Gyum; Dong, Zigang; Liu, Kangdong

doi:10.3389/fcell.2020.603472

Cited by 5 publications

(5 citation statements)

References 26 publications

(28 reference statements)

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“…Liu et al suggested that Honokiol had an anticancer function via directly interacting with keratin 18 protein in melanoma cells. The interaction between keratin 18 and Honokiol led to the degradation of keratin 18 by ubiquitination [ 25 ]. Another compound from ginger, 6-G, was also related with ubiquitination.…”

Section: Discussionmentioning

confidence: 99%

[6]-Paradol suppresses proliferation and metastases of pancreatic cancer by decreasing EGFR and inactivating PI3K/AKT signaling

et al. 2021

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Background The underlying mechanism behind the tumorigenesis and progression of pancreatic cancer is not clear, and treatment failure is generally caused by early metastasis, recurrence, drug resistance and vascular invasion. Exploring novel therapeutic regimens is necessary to overcome drug resistance and improve patients outcomes. Methods Functional assays were performed to investigate the role of [6]-Paradol (6-P) in proliferation and metastasis of pancreatic cancer in vitro and in vivo. The interaction between EGFR and 6-P was tested by KEGG enrichment analysis and molecular docking analysis. qRT-PCR was performed to detect the mRNA expression of EGFR in 6-P treated groups. Involvement of the PI3K/AKT pathway was measured by western blotting. Results 6-P significantly suppressed pancreatic cancer cell proliferation and metastasis. KEGG enrichment analysis and molecular docking analysis suggested that there existed certain interaction between EGFR and 6-P. In addition, 6-P obviously decreased EGFR protein expression level but did not change the mRNA expression level of EGFR. 6-P could induce degradation of EGFR through decreasing the protein stability of EGFR and enhancing the ubiquitin-mediated proteasome-dependent degradation, 6-P-mediated EGFR degradation led to inactivation of PI3K/AKT signaling pathway. However, ectopic expression of EGFR protein resulted in resistance to 6-P-mediated inactivity of PI3K/AKT signaling and inhibition of malignant phenotype of pancreatic cancer. Inversely, erlotinib could enhance the 6-P-mediated anticancer activity. Conclusion Our data indicated that 6-P/EGFR/PI3K/AKT signaling axis might become one of the potential therapies for the treatment of pancreatic cancer.

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Section: Discussionmentioning

confidence: 99%

[6]-Paradol suppresses proliferation and metastases of pancreatic cancer by decreasing EGFR and inactivating PI3K/AKT signaling

et al. 2021

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“…The interaction between keratin 18 and Honokiol led to the degradation of keratin 18 by ubiquitination. [25] Another compound from ginger, 6-G, was also related with ubiquitination. The study indicated 6-G decreased the expression of USP14, which was a ubiquitinspeci c peptidase mainly exerting inhibitory effect on ubiquitnation.…”

Section: Discussionmentioning

confidence: 99%

[6]-Paradol Suppresses Proliferation and Metastases of Pancreatic Cancer by Decreasing EGFR and Inactivating PI3K/AKT Signaling

Jiang

Wang

Chen

et al. 2021

Preprint

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Background: The underlying mechanism behind the tumorigenesis and progression of pancreatic cancer is not clear, and treatment failure is generally caused by early metastasis, recurrence, drug resistance and vascular invasion. Exploring novel therapeutic regimens is necessary to overcome drug resistance and improve patients outcomes.Methods: Functional assays were performed to investigated the role of 6-Paradol in proliferation and metastasis in vitro and vivo. The interaction between EGFR and 6-P was tested by KEGG enrichment analysis and molecular docking analysis. qRT-PCR was performed to detected the mRNA expression of EGFR in 6-P treated groups. Involvement of the PI3K/AKT pathway was measured by western blotting.Results: 6-P significantly suppressed pancreatic cancer cell proliferation and metastasis. KEGG enrichment analysis and molecular docking analysis suggested that there was an interaction between EGFR and 6-P. In addition, 6-P obviously decreased EGFR protein expression levels but did not change the mRNA of EGFR. 6-P could induce degradation of EGFR through decreasing the protein stability of EGFR and enhancing the ubiquitin-mediated proteasome-dependent degradation,6-P-mediated EGFR degradation led to inactivating PI3K/AKT signaling pathway. However, Ectopic expression of EGFR protein resulted in resistance to 6-P-mediated inactivity of PI3K/AKT signaling and inhibition of malignant phenotype. Inversely, erlotinib could enhance the 6-P-mediated anticancer activity. Conclusion: Our data indicated that 6-P/EGFR/PI3K/AKT signaling axis might become one of the supplemental therapeutic strategies for pancreatic cancer.

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“…Studies had shown that honokiol significantly inhibited melanoma cell's proliferation and viability, induced autophagy and apoptosis, 15 also inhibited the growth of melanoma cancer stem cells 16 . Besides in vitro studies, honokiol caused a significant reduction of tumor growth in melanoma xenogragts 17 . Moreover, honokiol could thwart the metastasis and migration of melanoma, 18,19 and be helpful to the drug resistance of melanoma.…”

Section: The Therapeutic Applications In Dermatosismentioning

confidence: 99%

“…16 Besides in vitro studies, honokiol caused a significant reduction of tumor growth in melanoma xenogragts. 17 Moreover, honokiol could thwart the metastasis and migration of melanoma, 18,19 and be helpful to the drug resistance of melanoma. It also can be used as a supplement to enhance the effects of other antimelanoma drugs.…”

Section: The Effects and Mechanisms In Melanomamentioning

confidence: 99%

The application prospects of honokiol in dermatology

Liang

Zhou

2022

Dermatologic Therapy

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Honokiol is one of the natural extracts of Magnolia officinalis. It is a small molecule, lipophilic compound with extensive biological effects. It has been used in the treatment of multisystem diseases, including digestive diseases, endocrine diseases, nervous system diseases, and various tumors. This paper reviews the biological effects of honokiol on the treatment of skin diseases in recent years, including antimicrobial, anti-oxidant, anti-inflammatory, anti-tumor, anti-fibrosis, anti-allergy, photo-protection, and immunomodulation. Most current researches are focused on the effects of anti-melanoma and photo-protection. Therefore, we summarized the specific mechanisms about these two effects. On the other side of treating skin diseases, the advantages of topical drugs cannot be replaced. As a small molecule fat-soluble compound, honokiol is suitable for external use. We reviewed the advantages and disadvantages of the topical mixed cream and various improved methods. These improvements include physical and chemical penetration enhancers, drug carriers, and chemical derivatives. In conclusion, honokiol has a wide range of effects, and its topical preparation provides a safe and effective way for treating skin diseases.

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Honokiol Inhibits Melanoma Growth by Targeting Keratin 18 in vitro and in vivo

Cited by 5 publications

References 26 publications

[6]-Paradol suppresses proliferation and metastases of pancreatic cancer by decreasing EGFR and inactivating PI3K/AKT signaling

[6]-Paradol suppresses proliferation and metastases of pancreatic cancer by decreasing EGFR and inactivating PI3K/AKT signaling

[6]-Paradol Suppresses Proliferation and Metastases of Pancreatic Cancer by Decreasing EGFR and Inactivating PI3K/AKT Signaling

The application prospects of honokiol in dermatology

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