&lt;p&gt;Lenvatinib for the treatment of unresectable hepatocellular carcinoma: evidence to date&lt;/p&gt;

Personeni, Nicola; Pressiani, Tiziana; Rimassa, Lorenza

doi:10.2147/jhc.s168953

Cited by 60 publications

(54 citation statements)

References 45 publications

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“…After bioinformatics prediction, we identified miR-3619-5p may be a target miRNA of DGCR5, and their direct interaction was confirmed by dual-luciferase assay. Previous studies have revealed that miR-3619-5p plays a tumor suppressive role in various cancers [19,36,37]. Then we conducted a series of loss/gain-of-function assays to explore the expression pattern and biological role of miR-3619-5p in GBC.…”

Section: Discussionmentioning

confidence: 99%

DGCR5 Promotes Gallbladder Cancer by Sponging MiR-3619-5p via MEK/ERK1/2 and JNK/p38 MAPK Pathways

et al. 2020

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Gallbladder cancer (GBC) is a highly aggressive malignant cancer with poor prognosis. Long noncoding RNA (lncRNA) DiGeorge syndrome critical region gene (DGCR5) has been reported to participate in various types of cancers, but its role in GBC remains largely unknown. This study aimed to explore the functions and mechanisms of DGCR5 in GBC. Here, we found that DGCR5 was upregulated in GBC tissues and cell lines. Through functional experiments, it was demonstrated that silence of DGCR5 significantly suppressed the cell proliferation, migration, invasion, and induced apoptosis and cell cycle arrest in GBC cells. In addition, miR-3619-5p was predicted and further verified as the target of DGCR5. Moreover, miR-3619-5p was observed downregulated in GBC tissues and cell lines, and miR-3619-5p mimics repressed the GBC cell proliferation, migration, invasion and could be rescued by DGCR5 overexpression. Mechanistically, it was found that DGCR5 knockdown and miR-3619-5p mimics inactivated the MEK/ERK1/2 and JNK/p38 MAPK pathways. In addition, rescue experiments indicated that inhibition of MEK/ERK1/2 and JNK/p38 MAPK pathways could reverse the effects of DGCR5 overexpression on cell proliferation, migration and invasion. Finally, xenograft model assay was used to validate that knockdown of DGCR5 suppressed GBC via regulating MEK/ERK1/2 and JNK/p38 MAPK pathways in vivo. Taken together, it was uncovered in our study that DGCR5 exerts an oncogenic role by sponging miR-3619-5p and activating MEK/ERK1/2 and JNK/p38 MAPK pathways in GBC progression.

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Section: Discussionmentioning

confidence: 99%

DGCR5 Promotes Gallbladder Cancer by Sponging MiR-3619-5p via MEK/ERK1/2 and JNK/p38 MAPK Pathways

et al. 2020

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“…Noticeably, the HCC incidence rates depend on the factors including race/ethnicity, gender, age, and geo‐/demographic regions and also by several risk factors such as cirrhosis, hepatitis B (HBV) infection, hepatitis C (HCV) infection, excessive alcohol consumption, nonalcoholic fatty liver disease (NAFLD), obesity, diabetes, glucose overload, metabolic syndrome, and environmental toxic intake (Fig. ) . The development of HCC is complex, involving sustained inflammatory damage leading to hepatocyte necrosis, regeneration, and fibrotic deposition.…”

Section: Introductionmentioning

confidence: 99%

Assessment of risk factors, and racial and ethnic differences in hepatocellular carcinoma

et al. 2020

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Despite improved screening and surveillance guidelines, significant race/ethnicity‐specific disparities in hepatocellular carcinoma (HCC) continue to exist and disproportionately affect minority and disadvantaged populations. This trend indicates that social determinants, genetic, and environmental factors are driving the epidemic at the population level. Race and geography had independent associations with risk of mortality among patients with HCC. The present review discusses the risk factors and issues related to disparities in HCC. The underlying etiologies for these disparities are complex and multifactorial. Some of the risk factors for developing HCC include hepatitis B (HBV) and hepatitis C (HCV) viral infection, nonalcoholic fatty liver disease, nonalcoholic steatohepatitis, smoking and alcohol consumption. In addition, population genetics; socioeconomic and health care access; treatment and prevention differences; and genetic, behavioral, and biological influences can contribute to HCC. Acculturation of ethnic minorities, insurance status, and access to health care may further contribute to the observed disparities in HCC. By increasing awareness, better modalities for screening and surveillance, improving access to health care, and adapting targeted preventive and therapeutic interventions, disparities in HCC outcomes can be reduced or eliminated.

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“…Sorafenib, a targeted drug, has been shown to be effective in prolonging HCC patient survival; however, the use of sorafenib is limited due to the high cost. 38 Therefore, it is very meaningful to screen out a drug that can improve the sensitivity of sorafenib. Studies had shown that SK enhanced the sensitivity of non-small cell lung cancer to erlotinib and gefitinib.…”

Section: Discussionmentioning

confidence: 99%

<p>Experimental Study of Hepatocellular Carcinoma Treatment by Shikonin Through Regulating PKM2</p>

Liu

et al. 2020

JHC

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These authors contributed equally to this workObjective: Shikonin is a natural product with many activities, including anti-cancer effects. Pyruvate kinase type M2 (PKM2) plays a crucial role in the growth of tumor cells. However, the effect of shikonin on PKM2 in hepatocellular carcinoma (HCC) is unclear. Methods: Cell viability, apoptosis level, glucose uptake, and lactate production were detected in HCC cells. Lentivirus-overexpressed and -shRNA of PKM2 were used to verify the key target of shikonin. A xenograft mouse model was used to detect the efficacy of shikonin and its combination with sorafenib in vivo. Results: Shikonin inhibited proliferation and glycolysis and induced apoptosis in HCC cells. Either PKM2-overexpressed or PKM2-shRNA alleviated or enhanced this effect. The results of CCK-8 showed that shikonin significantly inhibited cell viability of HCC cells. The levels of glucose uptake and lactate production were dramatically decreased by shikonin-treated. Results of flow cytometry and Western blot showed that the levels of apoptosis of HCC cells were significantly increased in a dose-dependent manner after shikonin treatment. In addition, shikonin enhanced the anti-cancer effect of sorafenib in vitro and in vivo. Our results showed that SK combined with sorafenib markedly inhibits tumor growth in HCCtransplanted nude mice compared to SK or sorafenib alone. Conclusion: By inhibiting PKM2, shikonin inhibited proliferation and glycolysis and induced cell apoptosis in HCC cells. The effect of shikonin on tumor cell proliferation, apoptosis and glycolsis will make it promising drug for HCC patients.

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<p>Lenvatinib for the treatment of unresectable hepatocellular carcinoma: evidence to date</p>

Cited by 60 publications

References 45 publications

DGCR5 Promotes Gallbladder Cancer by Sponging MiR-3619-5p via MEK/ERK1/2 and JNK/p38 MAPK Pathways

DGCR5 Promotes Gallbladder Cancer by Sponging MiR-3619-5p via MEK/ERK1/2 and JNK/p38 MAPK Pathways

Assessment of risk factors, and racial and ethnic differences in hepatocellular carcinoma

<p>Experimental Study of Hepatocellular Carcinoma Treatment by Shikonin Through Regulating PKM2</p>

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