The tyrosine kinase inhibitor sorafenib sensitizes hepatocellular carcinoma cells to taxol by suppressing the HURP protein

Kuo, Tsung-Cheng; Lu, Hsing-Pang; Chao, Chuck C.‐K.

doi:10.1016/j.bcp.2011.04.008

Cited by 29 publications

(20 citation statements)

References 55 publications

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“…The proteasomal function is important for NF-kB activation, and NF-kB seems to regulate the expression of BUB1 [60], DLGAP5 [61] and AURKB [62]. Altered proteasomal function may thus contribute to NF-kB activation and thereby increase the expression of at least three of the genes showing increased expression in AML cells with prolonged in vitro proliferation.…”

Section: Discussionmentioning

confidence: 94%

Identification of a subset of patients with acute myeloid leukemia characterized by long-termin vitroproliferation and altered cell cycle regulation of the leukemic cells

Hatfield

Reikvam

Bruserud

2014

Expert Opinion on Therapeutic Targets

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Section: Discussionmentioning

confidence: 94%

Identification of a subset of patients with acute myeloid leukemia characterized by long-termin vitroproliferation and altered cell cycle regulation of the leukemic cells

Hatfield

Reikvam

Bruserud

2014

Expert Opinion on Therapeutic Targets

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“…ERK is activated in HepG 2 cells after treatment with HGF and constitutive expression of Ha-Ras (35,36). ERK inhibitor is suggested as a potential anti-HCC agent (37)(38)(39). Sorafenib is the first targeted therapy drug that has demonstrated an improved overall survival benefit in patients with advanced HCC (40)(41)(42).…”

Section: Discussionmentioning

confidence: 99%

Preferential inhibition of hepatocellular carcinoma by the flavonoid Baicalein through blocking MEK-ERK signaling

Liang

Zhang

et al. 2012

International Journal of Oncology

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Abstract. Baicalein is a purified flavonoid extracted from the roots of Scutellaria baicalensis or Scutellaria radix. Although previous studies have suggested that Baicalein possesses an in vitro anti-hepatocellular carcinoma activity, its in vivo effects and mechanisms of action are still not completely understood. In this study, Baicalein at concentrations of 40-120 µM exhibited significant cytotoxicity to three hepatocellular carcinoma (HCC) cell lines but marginal cytotoxicity to a normal liver cell line in vitro. Compared to a standard chemotherapy drug, 5-fluorouracil (5-FU), Baicalein had greater effect on HCC cells but less toxicity on normal liver cells. Treatment with Baicalein dramatically reduced mitochondrial transmembrane potential, and activated caspase-9 and caspase-3. Blockade of Baicaleininduced apoptosis with a pan-caspase inhibitor partially attenuated Baicalein-induced growth inhibition in HCC. Baicalein treatment significantly inhibited tumor growth of HCC xenografts in mice. Induction of apoptosis was demonstrated in Baicalein-treated xenograft tumors by the terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. Furthermore, Baicalein treatment dramatically decreased the levels of phosphorylation of MEK1, ERK1/2 and Bad in vitro and in vivo. Overexpression of human MEK1 partially blocked Baicalein-induced growth inhibition. Consequently, these findings suggest that Baicalein preferentially inhibits HCC tumor growth through inhibition of MEK-ERK signaling and by inducing intrinsic apoptosis. IntroductionHepatocellular carcinoma (HCC) is one of the common cancers in Asia and Africa. The incidence of HCC is increasing in Europe and the United States (1). Although HCC can be cured at the early stage by surgical resection, most patients can not be diagnosed at the early stage since tumors are asymptomatic (2). Current treatment options for HCC patients at the late stage include chemotherapy, chemoembolization, ablation, and proton beam therapy. These treatment options remain disappointed in clinic. HCC patients will relapse and rapidly progress to the advanced stages with vascular invasion and multiple metastases, which lead to a low 5-year survival rate of less than 7% (3). HCC patients who have surgically resectable localized tumors show a better prognosis. However, even these patients have a dismal 5-year survival rate of 15 to 39% (4). Clearly, there is an urgent need to search for new therapies for this lethal disease.We have reported that chrysanthemum indicum extract (CIE), a Chinese herbal extraction, exerts a significantly inhibitory effect on HCC cells (MHCC97H) in previous studies (5,6). One particular point to stress is that CIE appeares to have no cytotoxic effect on normal liver cells, highlighting an advantage of the herbal treatment. Herbal medicine flavonoids have recently received increasing attention because of the beneficial effects of anti-tumor and

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“…Most of the chemotherapeutic drugs, such as taxol, epirubicin, cisplatin, 5‐fluorouracil and etoposide, either individually or in combination, have relatively low efficacy in treating HCC . Great efforts have been made to unveil the mechanisms underlying the insensitivity of HCC cells to chemotherapies, such as MTA . One main cause that confers MTA resistance to HCC cells is the mitotic checkpoint bypass .…”

Section: Introductionmentioning

confidence: 99%

“…2 Great efforts have been made to unveil the mechanisms underlying the insensitivity of HCC cells to chemotherapies, such as MTA. 3,4 One main cause that confers MTA resistance to HCC cells is the mitotic checkpoint bypass. 5 For example, the regulation of SAC, which controls cell cycle progression during mitosis and synchronizes mitosis by attaching chromosomes to spindle microtubules, 6 is critical for taxol-mediated cell death.…”

Section: Introductionmentioning

confidence: 99%

Inhibition of kinesin family member 20B sensitizes hepatocellular carcinoma cell to microtubule‐targeting agents by blocking cytokinesis

Liu

Zhang

et al. 2018

Cancer Science

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Kinesin family member 20B (KIF20B, also known as MPHOSPH1) is a kinesin protein that plays a critical role in cytokinesis. Previously, we and others have demonstrated the oncogenic role of KIF20B in several cancers; however, the exact mechanisms underlying its tumorigenic effects remain unclear. Herein, we showed overexpression of KIF20B in human hepatocellular carcinoma (HCC) and reported a negative correlation between KIF20B level and prognosis of patients. Mechanistically, reducing KIF20B blockades mitotic exit of HCC cells at telophase in a spindle assembly checkpoint independent way. Importantly, reducing KIF20B acts synergistically with three microtubule‐associated agents (MTA) to p53‐ or p14ARF‐dependently suppress p53‐wt or p53‐null HCC cells. In addition to taxol, reducing KIF20B also enhanced the toxicity of two chemotherapeutic drugs, hydroxycamptothecin and mitomycin C. In conclusion, we found a novel mechanism in that blocking cytokinesis by KIF20B inhibition increases the efficacy of MTA; our results thus suggested a dual‐mitotic suppression approach against HCC by combining MTA with KIF20B inhibition, which simultaneously blocks mitosis at both metaphase and telophase.

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The tyrosine kinase inhibitor sorafenib sensitizes hepatocellular carcinoma cells to taxol by suppressing the HURP protein

Cited by 29 publications

References 55 publications

Identification of a subset of patients with acute myeloid leukemia characterized by long-termin vitroproliferation and altered cell cycle regulation of the leukemic cells

Identification of a subset of patients with acute myeloid leukemia characterized by long-termin vitroproliferation and altered cell cycle regulation of the leukemic cells

Preferential inhibition of hepatocellular carcinoma by the flavonoid Baicalein through blocking MEK-ERK signaling

Inhibition of kinesin family member 20B sensitizes hepatocellular carcinoma cell to microtubule‐targeting agents by blocking cytokinesis

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