Honokiol induces caspase-independent paraptosis via reactive oxygen species production that is accompanied by apoptosis in leukemia cells

Wang, Yao; Yang, Zehong; Zhao, Xiaojun

doi:10.1016/j.bbrc.2012.12.063

Cited by 36 publications

(20 citation statements)

References 23 publications

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“…The caspase independent PCD are autophagy, mitotic catastrophe, paraptosis, exitotoxicity, Wallerian degeneration and programmed necrosis [4]. Many natural anti-cancer substances such as taxol [3], [32], yessotoxin [14], ginsenoside [20], curcumin [40], honoki [36], γ-tocotrienol [42] can induce caspase independent PCD besides the caspase dependent one. The cytotoxic effect of hesperidin triggering non apoptotic mechanisms is not well understood.…”

Section: Discussionmentioning

confidence: 99%

Hesperidin Induces Paraptosis Like Cell Death in Hepatoblatoma, HepG2 Cells: Involvement of ERK1/2 MAPK

et al. 2014

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Hesperidin, a natural flavonoid abundantly present in Citrus is known for its anti-cancer, anti-oxidant and anti-inflammatory properties. In this study we examined the effect of hesperidin on HepG2 cells. HepG2 cells treated with various concentration of hesperidin undergo a distinct type of programed cell death. Cytoplasmic vacuolization, mitochondria and endoplasmic reticulum swelling and uncondensed chromatin were observed in hesperidin treated cells. DNA electrophoresis show lack of DNA fragmentation and western blot analysis demonstrates lack of caspase activation and PARP cleavage. It was observed that hesperidin induced cell death is nonautophagic and also activate mitogen activated protein kinase ERK1/2. Taken together, the data indicate that hesperidin induces paraptosis like cell death in HepG2 cells with the activation of ERK1/2. Thus our finding suggests that hesperidin inducing paraptosis may offer an alternative tool in human liver carcinoma therapy.

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Section: Discussionmentioning

confidence: 99%

Hesperidin Induces Paraptosis Like Cell Death in Hepatoblatoma, HepG2 Cells: Involvement of ERK1/2 MAPK

et al. 2014

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“…The effect of honokiol is similar to that of curcumin: it was also shown to promote mPTP opening and ROS accumulation [111]; although honokiol inhibits rather than induces MAPK/ERK signaling [112, 113] (Figure 2). Similar to IGF1R, curcumin and honokiol activities are suppressed by Alix/AIP1 overexpression, inhibitors of transcription/translation, antioxidants, and inhibitors of the JNK/SAPK and (for curcumin) MAPK/ERK pathways [94, 103, 114]. …”

Section: Vacuolization and Known Cell Death Pathwaysmentioning

confidence: 99%

Cytoplasmic vacuolization in cell death and survival

et al. 2016

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Cytoplasmic vacuolization (also called cytoplasmic vacuolation) is a well-known morphological phenomenon observed in mammalian cells after exposure to bacterial or viral pathogens as well as to various natural and artificial low-molecular-weight compounds. Vacuolization often accompanies cell death; however, its role in cell death processes remains unclear. This can be attributed to studying vacuolization at the level of morphology for many years. At the same time, new data on the molecular mechanisms of the vacuole formation and structure have become available. In addition, numerous examples of the association between vacuolization and previously unknown cell death types have been reported. Here, we review these data to make a deeper insight into the role of cytoplasmic vacuolization in cell death and survival.

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“…Silencing of p53 reduced the ability of Rh2 to induce vacuole formation characteristic for paraptosis [317]. Honokiol from Magnolia officinalis can induce paraptosis in human leukemia NB4 cells [318]. Hesperidin, a flavanone glycoside found in citrus fruits, induced paraptotic cell death in human hepatocellular carcinoma HepG2 cells [319].…”

Section: Natural Compounds and Other Cell Death Pathwaysmentioning

confidence: 99%

Natural Compounds As Modulators of Non-apoptotic Cell Death in Cancer Cells

Guamán-Ortiz

Orellana²,

Ratovitski³

2017

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Cell death is an innate capability of cells to be removed from microenvironment, if and when they are damaged by multiple stresses. Cell death is often regulated by multiple molecular pathways and mechanism, including apoptosis, autophagy, and necroptosis. The molecular network underlying these processes is often intertwined and one pathway can dynamically shift to another one acquiring certain protein components, in particular upon treatment with various drugs. The strategy to treat human cancer ultimately relies on the ability of anticancer therapeutics to induce tumor-specific cell death, while leaving normal adjacent cells undamaged. However, tumor cells often develop the resistance to the drug-induced cell death, thus representing a great challenge for the anticancer approaches. Numerous compounds originated from the natural sources and biopharmaceutical industries are applied today in clinics showing advantageous results. However, some exhibit serious toxic side effects. Thus, novel effective therapeutic approaches in treating cancers are continued to be developed. Natural compounds with anticancer activity have gained a great interest among researchers and clinicians alike since they have shown more favorable safety and efficacy then the synthetic marketed drugs. Numerous studies in vitro and in vivo have found that several natural compounds display promising anticancer potentials. This review underlines certain information regarding the role of natural compounds from plants, microorganisms and sea life forms, which are able to induce non-apoptotic cell death in tumor cells, namely autophagy and necroptosis.

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Honokiol induces caspase-independent paraptosis via reactive oxygen species production that is accompanied by apoptosis in leukemia cells

Cited by 36 publications

References 23 publications

Hesperidin Induces Paraptosis Like Cell Death in Hepatoblatoma, HepG2 Cells: Involvement of ERK1/2 MAPK

Hesperidin Induces Paraptosis Like Cell Death in Hepatoblatoma, HepG2 Cells: Involvement of ERK1/2 MAPK

Cytoplasmic vacuolization in cell death and survival

Natural Compounds As Modulators of Non-apoptotic Cell Death in Cancer Cells

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