• Bioactivity
• Chemical structure
• Ginsenosides Rg3
• Ginsenosides Rh2
• Rare ginsenosides

• Ginsenosides/pharmacology
• Ginsenosides/chemistry
• Panax/chemistry
• Humans
• Anti-Bacterial Agents/pharmacology
• Anti-Bacterial Agents/chemistry
• Animals

• anti-hepatocellular carcinoma
• ginsenoside Rb1
• ginsenoside Rd
• ginsenoside Rg3
• ginsenoside Rg5
• ginsenoside Rh2
• ginsenoside Rk1
• network pharmacology
• protopanaxadiol ginsenosides

• autophagy inhibitors
• cancer therapy
• clinical trials

• Humans
• Autophagy/drug effects
• Neoplasms/drug therapy
• Neoplasms/pathology
• Neoplasms/metabolism
• Animals
• Antineoplastic Agents/pharmacology
• Antineoplastic Agents/therapeutic use
• Chloroquine/pharmacology
• Chloroquine/therapeutic use
• Hydroxychloroquine/therapeutic use
• Hydroxychloroquine/pharmacology

• 2020B1212030006 The Science and Technology Development Fund, Macau SAR (0024/2020/A1, SKL-QRCM(UM)-2023-2025) and the 2020 Guangdong Provincial Science and Technology Innovation Strategy Special Fund (Guangdong-Hong Kong-Macau Joint Lab)

• Ginsenoside Rk1
• PI3K/Akt/mTOR pathway
• RNA sequencing
• Radiation-induced intestinal injury
• Radioprotective

• Rats
• Animals
• Proto-Oncogene Proteins c-akt/metabolism
• Phosphatidylinositol 3-Kinases/metabolism
• TOR Serine-Threonine Kinases/metabolism
• Signal Transduction
• Apoptosis
• Radiation Injuries/drug therapy
• Radiation Injuries/prevention & control

Cancer is one of the leading causes of death globally. The development of drug resistance is the main contributor to cancer-related mortality. Cancer cells exploit multiple mechanisms to reduce the therapeutic effects of anticancer drugs, thereby causing chemotherapy failure. Natural products are accessible, inexpensive, and less toxic sources of chemotherapeutic agents. Additionally, they have multiple mechanisms of action to inhibit various targets involved in the development of drug resistance. In this review, we have summarized the basic research and clinical applications of natural products as possible inhibitors for drug resistance in cancer. The molecular targets and the mechanisms of action of each natural product are also explained. Diverse drug resistance biomarkers were sensitive to natural products. P-glycoprotein and breast cancer resistance protein can be targeted by a large number of natural products. On the other hand, protein kinase C and topoisomerases were less sensitive to most of the studied natural products. The studies discussed in this review will provide a solid ground for scientists to explore the possible use of natural products in combination anticancer therapies to overcome drug resistance by targeting multiple drug resistance mechanisms.

• anticancer natural products
• drug detoxification
• drug efflux
• plants derived natural products

• Apoptosis
• Autophagy
• Cancer therapy
• Endoplasmic reticulum stress
• Ginsenoside

Autophagy is a vacuolar, lysosomal degradation pathway for injured and damaged protein molecules and organelles in eukaryotic cells, which is controlled by nutrients and stress responses. Dysregulation of cellular autophagy may lead to various diseases such as neurodegenerative disease, obesity, cardiovascular disease, diabetes, and malignancies. Recently, natural compounds have come to attention for being able to modulate the autophagy pathway in cancer prevention, although the prospective role of autophagy in cancer treatment is very complex and not yet clearly elucidated. Numerous synthetic chemicals have been identified that modulate autophagy and are favorable candidates for cancer treatment, but they have adverse side effects. Therefore, different phytochemicals, which include natural compounds and their derivatives, have attracted significant attention for use as autophagy modulators in cancer treatment with minimal side effects. In the current review, we discuss the promising role of natural compounds in modulating the autophagy pathway to control and prevent cancer, and provide possible therapeutic options.

• autophagy
• cancer
• natural compound
• phytochemical
• treatment

• Autophagy
• activate
• anticancer
• cancer
• inhibit
• natural products.

• HEK-293
• anti-apoptosis
• cisplatin
• ginsenoside Rk1
• nephrotoxicity

The Panax ginseng berry extract (GBE) is well known to have an antidiabetic effect. The aim of this study is to evaluate and investigate the protective effect of ultrasonication-processed P. ginseng berry extract (UGBE) compared with GBE on liver fibrosis induced by mild bile duct ligation (MBDL) model in rats. After ultrasonication process, the composition ratio of ginsenoside in GBE was changed. The component ratio of ginsenosides Rh1, Rh4, Rg2, Rg3, Rk1, Rk3, and F4 in the extract was elevated.

In this study, the protective effect of the newly developed UGBE was evaluated on hepatotoxicity and neuronal damage in MBDL model. Silymarin (150 mg/kg) was used for positive control. UGBE (100 mg/kg, 250 mg/kg, 500 mg/kg), GBE (250 mg/kg), and silymarin (150 mg/kg) were orally administered for 6 weeks after MBDL surgery.

The MBDL surgery induced severe hepatotoxicity that leads to liver inflammation in rats. Also, the serum ammonia level was increased by MBDL surgery. However, the liver dysfunction of MBDL surgery–operated rats was attenuated by UGBE treatment via myeloid differentiation factor 88-dependent Toll-like receptor 4 signaling pathways.

UGBE has a protective effect on liver fibrosis induced by MBDL in rats through inhibition of the TLR4 signaling pathway in liver.

• Acute liver failure
• Ginseng berry
• Hepatotoxicity
• Toll-like receptor 4
• Ultrasonication

• Autophagy
• Endoplasmic reticulum stress
• Non-small cell lung cancer
• Total ginsenoside extract

• Activating Transcription Factor 4/metabolism
• Antineoplastic Agents/pharmacology
• Autophagic Cell Death/drug effects
• Carcinoma, Non-Small-Cell Lung/drug therapy
• Carcinoma, Non-Small-Cell Lung/metabolism
• Cell Line, Tumor
• Endoplasmic Reticulum Stress/drug effects
• Ginsenosides/pharmacology
• Humans
• Lung Neoplasms/drug therapy
• Lung Neoplasms/metabolism
• Proto-Oncogene Proteins c-akt/metabolism
• TOR Serine-Threonine Kinases/metabolism
• Transcription Factor CHOP/metabolism

• Bioavailability
• Ginsenosides
• Pharmacokinetic
• Protopanaxadiol
• Protopanaxatriol

• autophagy
• cirrhosis
• fibrosis
• hepatitis
• hepatocellular carcinoma
• liver
• liver disease
• selective autophagy
• steatosis

• Animals
• Autophagy
• Disease Progression
• Humans
• Liver/metabolism
• Liver/physiology
• Liver Diseases/metabolism
• Liver Diseases/pathology
• Signal Transduction
• Vacuoles/metabolism

• Functional mechanism
• Ginsenosides
• Tumor growth
• Tumor metastasis

A green solvent extraction technology involving a microwave processing method was used to increase the content of minor ginsenosides from Panax notoginseng. This article aims to investigate the optimization of preparation of the minor ginsenosides by this microwave processing method using single-factor experiments and response surface methodology (RSM), and discuss the blood-enriching activity and hemostatic activity of the extract of microwave processed P. notoginseng (EMPN) The RSM for production of the minor ginsenosides was based on a three-factor and three-level Box-Behnken design. When the optimum conditions of microwave power, temperature and time were 495.03 W, 150.68 °C and 20.32 min, respectively, results predicted that the yield of total minor ginsenosides (Y₉) would be 93.13%. The actual value of Y₉ was very similar to the predicted value. In addition, the pharmacological results of EMPN in vivo showed that EMPN had the effect of enriching blood in N-acetylphenylhydrazine (APH) and cyclophosphamide (CTX)-induced blood deficient mice because of the increasing content of white blood cells (WBCs) and hemoglobin (HGB) in blood. Hemostatic activity in vitro of EMPN showed that it had significantly shortened the clotting time in PT testing (p < 0.05). The hemostatic effect of EMPN was mainly caused by its components of Rh₄, 20(S)-Rg₃ and 20(R)-Rg₃. This microwave processing method is simple and suitable to mass-produce the minor ginsenosides from P. notoginseng.

• blood-enriching activity
• hemostatic activity
• microwave processing
• minor ginsenosides
• response surface methodology

• Autophagy
• Cancer
• Cell death
• Oxidative stress
• Phytochemical
• Therapy

• Clinical pharmacology
• Ginsenoside
• Rk1
• Systematic review

• acute liver failure
• ginseng berry
• hepatotoxicity
• toll-like receptor 4
• ultrasonication

Frequent overdose of paracetamol (APAP) has become the major cause of acute liver injury. The present study was designed to evaluate the potential protective effects of ginsenoside Rk1 on APAP-induced hepatotoxicity and investigate the underlying mechanisms for the first time.

Mice were treated with Rk1 (10 mg/kg or 20 mg/kg) by oral gavage once per d for 7 d. On the 7th d, all mice treated with 250 mg/kg APAP exhibited severe liver injury after 24 h, and hepatotoxicity was assessed.

Our results showed that pretreatment with Rk1 significantly decreased the levels of serum alanine aminotransferase, aspartate aminotransferase, tumor necrosis factor, and interleukin-1β compared with the APAP group. Meanwhile, hepatic antioxidants, including superoxide dismutase and glutathione, were elevated compared with the APAP group. In contrast, a significant decrease in levels of the lipid peroxidation product malondialdehyde was observed in the ginsenoside Rk1-treated group compared with the APAP group. These effects were associated with a significant increase of cytochrome P450 E1 and 4-hydroxynonenal levels in liver tissues. Moreover, ginsenoside Rk1 supplementation suppressed activation of apoptotic pathways by increasing Bcl-2 and decreasing Bax protein expression levels, which was shown using western blotting analysis. Histopathological observation also revealed that ginsenoside Rk1 pretreatment significantly reversed APAP-induced necrosis and inflammatory infiltration in liver tissues. Biological indicators of nitrative stress, such as 3-nitrotyrosine, were also inhibited after pretreatment with Rk1 compared with the APAP group.

The results clearly suggest that the underlying molecular mechanisms in the hepatoprotection of ginsenoside Rk1 in APAP-induced hepatotoxicity may be due to its antioxidation, antiapoptosis, anti-inflammation, and antinitrative effects.

• APAP-induced hepatotoxicity
• anti-apoptosis
• anti-inflammation
• ginsenoside Rk1
• oxidative stress

Ginseng is a natural product best known for its curative properties in diverse physiological processes such as cancer, neurodegenerative disorders, hypertension, and maintenance of hemostasis in the immune system. In previous decades, there have been some promising studies into the pharmacology and chemistry of ginseng components and the relationship between their structure and function. The emerging use of modified ginseng and development of new compounds from ginseng for clinical studies have been topics of study for many researchers. The present review deals with the anticancer, anti-inflammatory, antioxidant, and chemopreventive effects, and recent advances in microRNA technology related to red ginseng. The review also summarizes the current knowledge on the effect of ginsenosides in the treatment of cancer.

• Panax ginseng
• anticancer activity
• ginseng-derived compounds
• ginsenosides

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.

• Autophagy
• Cancer
• Natural compounds
• Necroptosis
• Paraptosis

• AMPK
• Alzheimer's disease
• amyloid
• autophagy induction
• ginsenoside
• glycoconjugate
• insulin resistance
• medicinal plant
• phytochemical

• Apoptosis
• Autophagy
• Chemoresistance
• Gemcitabine
• Lung cancer

• DNA damage checkpoint
• NADPH oxidases
• ROS
• autophagic flux
• chemoresistance
• esophageal cancer
• estrogen receptor
• ginsenoside Ro

• Animals
• Apoptosis
• Autophagosomes/metabolism
• Autophagy
• Cell Cycle
• Cell Survival
• Checkpoint Kinase 1/metabolism
• Chlorocebus aethiops
• DNA Damage
• Esophageal Neoplasms/metabolism
• Estrogen Receptor beta/metabolism
• Fluorouracil/pharmacology
• Ginsenosides/chemistry
• Green Fluorescent Proteins/metabolism
• Humans
• Lysosomes/metabolism
• Mice
• NADPH Oxidases/metabolism
• Reactive Oxygen Species/metabolism
• Vero Cells

Hepatocellular carcinoma (HCC) is the second leading cause of cancer-related deaths worldwide. High mortality from HCC is mainly due to widespread prevalence and the lack of effective treatment, since systemic chemotherapy is ineffective, while the targeted agent Sorafenib extends median survival only briefly. The steroidal saponin 20(S)-ginsenoside Rg₃ from Panax ginseng C.A. Meyer is proposed to chemosensitize to various therapeutic drugs through an unknown mechanism. Since autophagy often serves as cell survival mechanism in cancer cells exposed to chemotherapeutic agents, we examined the ability of Rg₃ to inhibit autophagy and chemosensitize HCC cell lines to doxorubicin in vitro. We show that Rg₃ inhibits late stage autophagy, possibly through changes in gene expression. Doxorubicin-induced autophagy plays a protective role in HCC cells, and therefore Rg₃ treatment synergizes with doxorubicin to kill HCC cell lines, but the combination is relatively nontoxic in normal liver cells. In addition, Rg₃ was well-tolerated in mice and synergized with doxorubicin to inhibit tumor growth in HCC xenografts in vivo. Since novel in vivo inhibitors of autophagy are desirable for clinical use, we propose that Rg3 is such a compound, and that combination therapy with classical chemotherapeutic drugs may represent an effective therapeutic strategy for HCC treatment.

• Agaricales/chemistry
• Antineoplastic Agents/pharmacology
• Antineoplastic Combined Chemotherapy Protocols/pharmacology
• Apoptosis/drug effects
• Autophagy/drug effects
• Cell Line, Tumor
• Cell Proliferation/drug effects
• Drug Synergism
• Fluorouracil/pharmacology
• Humans
• Microtubule-Associated Proteins/drug effects
• Phellinus
• Plant Extracts
• Polysaccharides/pharmacology
• Triple Negative Breast Neoplasms/drug therapy
• Triple Negative Breast Neoplasms/pathology

• Dammarane saponin
• Damulin C
• Damulin D
• Gynostemma pentaphyllum
• HepG2 cell cytotoxic activity

• Antineoplastic Agents, Phytogenic/chemistry
• Antineoplastic Agents, Phytogenic/isolation & purification
• Antineoplastic Agents, Phytogenic/pharmacology
• Cell Proliferation/drug effects
• Dose-Response Relationship, Drug
• Drug Screening Assays, Antitumor
• Gynostemma/chemistry
• Hep G2 Cells
• Humans
• Molecular Structure
• Saponins/chemistry
• Saponins/isolation & purification
• Saponins/pharmacology
• Structure-Activity Relationship
• Triterpenes/chemistry
• Triterpenes/isolation & purification
• Triterpenes/pharmacology
• Dammaranes

Sun ginseng (SG), a specific formulation of quality-controlled red ginseng, contains approximately equal amounts of three major ginsenosides (RK1, Rg3, and Rg5), which reportedly has antitumor-promoting activities in animal models.

MTT assay was used to assess whether SG can potentiate the anticancer activity of epirubicin or paclitaxel in human cervical adenocarcinoma HeLa cells, human colon cancer SW111C cells, and SW480 cells; apoptosis status was analyzed by annexin V-FITC and PI and analyzed by flow cytometry; and apoptosis pathway was studied by analysis of caspase-3, -8, and -9 activation, mitochondrial accumulation of Bax and Bak, and cytochrome c release.

SG remarkably enhances cancer cell death induced by epirubicin or paclitaxel in human cervical adenocarcinoma HeLa cells, human colon cancer SW111C cells, and SW480 cells. Results of the mechanism study highlighted the cooperation between SG and epirubicin or paclitaxel in activating caspase-3 and -9 but not caspase-8. Moreover, SG significantly increased the mitochondrial accumulation of both Bax and Bak triggered by epirubicin or paclitaxel as well as the subsequent release of cytochrome c in the targeted cells.

SG significantly potentiated the anticancer activities of epirubicin and paclitaxel in a synergistic manner. These effects were associated with the increased mitochondrial accumulation of both Bax and Bak that led to an enhanced cytochrome c release, caspase-9/-3 activation, and apoptosis. Treating cancer cells by combining epirubicin and paclitaxel with SG may prove to be a novel strategy for enhancing the efficacy of the two drug types.

• apoptosis
• caspase-9
• sun ginseng
• synergistic effect

• Epithelial–mesenchymal transition (EMT)
• Ginsenoside 20(R)-Rg3
• Lung cancer
• Metastasis
• Transforming growth factor-beta 1 (TGF-β1)

• chloroquine
• cirrhosis
• hepatic
• ischemia
• non-alcoholic fatty liver disease

• autophagy
• hepatocellular carcinoma
• metastasis
• target therapy
• tissue-specific

• Animals
• Anoikis/drug effects
• Anoikis/genetics
• Apoptosis Regulatory Proteins/antagonists & inhibitors
• Apoptosis Regulatory Proteins/genetics
• Autophagy/drug effects
• Autophagy/genetics
• Autophagy-Related Protein 5
• Beclin-1
• Carcinoma, Hepatocellular/genetics
• Carcinoma, Hepatocellular/pathology
• Carcinoma, Hepatocellular/therapy
• Cell Line, Tumor
• Cell Movement/drug effects
• Cell Movement/genetics
• Down-Regulation/drug effects
• Down-Regulation/genetics
• HeLa Cells
• Hep G2 Cells
• Humans
• Liver Neoplasms/genetics
• Liver Neoplasms/pathology
• Liver Neoplasms/therapy
• Lung Neoplasms/genetics
• Lung Neoplasms/prevention & control
• Lung Neoplasms/secondary
• Male
• Mice
• Mice, Inbred BALB C
• Mice, Nude
• Microtubule-Associated Proteins/antagonists & inhibitors
• Microtubule-Associated Proteins/genetics
• RNA, Small Interfering/pharmacology
• Xenograft Model Antitumor Assays

• Autophagy
• Cancer
• Complementary therapy
• Garlic

• Apoptosis/drug effects
• Apoptosis/genetics
• Autophagy/drug effects
• Autophagy/genetics
• Autophagy-Related Proteins
• Carcinoma, Hepatocellular/drug therapy
• Carcinoma, Hepatocellular/genetics
• Carcinoma, Hepatocellular/metabolism
• Carcinoma, Hepatocellular/pathology
• Cell Line, Tumor
• Cisplatin/pharmacology
• Cysteine Endopeptidases/genetics
• Cysteine Endopeptidases/metabolism
• Hep G2 Cells
• Humans
• Liver Neoplasms/drug therapy
• Liver Neoplasms/genetics
• Liver Neoplasms/metabolism
• Liver Neoplasms/pathology
• MicroRNAs/genetics
• MicroRNAs/metabolism
• Stathmin/genetics
• Stathmin/metabolism
• TOR Serine-Threonine Kinases/genetics
• TOR Serine-Threonine Kinases/metabolism
• rab5 GTP-Binding Proteins/genetics
• rab5 GTP-Binding Proteins/metabolism

• Annexin A5
• Apoptosis/drug effects
• Autophagy/drug effects
• Blotting, Western
• Cell Cycle/drug effects
• Cell Line, Tumor
• Cell Survival/drug effects
• Diosgenin/analogs & derivatives
• Diosgenin/pharmacology
• Fluorescent Antibody Technique
• Fluorescent Dyes
• Humans
• Indoles
• Lung Neoplasms/pathology
• MAP Kinase Kinase 4/drug effects
• MAP Kinase Signaling System/drug effects
• Oncogene Protein v-akt/physiology
• Organelles/drug effects
• Phosphatidylinositol 3-Kinases/physiology
• Signal Transduction/drug effects

Our previous study has revealed that dioscin, a compound with anti-inflammatory, lipid-lowering, anticancer and hepatoprotective effects, may induce autophagy in hepatoma cells. Autophagy is a lysosomal degradation pathway that is essential for cell survival and tissue homeostasis. In this study, the role of autophagy and related signaling pathways during dioscin-induced apoptosis in human lung cancer cells was investigated. Results from 4′-6-diamidino-2-phenylindole and annexin-V/PI double-staining assay showed that caspase-3- and caspase-8-dependent, and dose-dependent apoptoses were detected after a 24-h dioscin treatment. Meanwhile, autophagy was detected as early as 12 h after an exposure to low-dose dioscin, as indicated by an up-regulated expression of LC3-II and beclin-1 proteins. Blockade of autophagy with bafilomycin A1 or 3-methyladenine sensitized the A549 and H1299 cells to apoptosis. Treatment of A549 and H1299 cells with dioscin caused a dose-dependent increase in ERK1/2 and JNK1/2 activity, accompanied with a decreased PI3K expression and decreased phosphorylation of Akt and mTOR. Taken together, this study demonstrated for the first time that autophagy occurred earlier than apoptosis during dioscin-induced human lung cancer cell line apoptosis. Dioscin-induced autophagy via ERK1/2 and JNK1/2 pathways may provide a protective mechanism for cell survival against dioscin-induced apoptosis to act as a cytoprotective reaction.

• valproic acid
• autophagy
• prostate cancer
• atg5
• lc3
• du145 cells
• lncap cells
• pc-3 cells

• Adaptor Proteins, Signal Transducing/metabolism
• Alternative Splicing/drug effects
• Autophagy/drug effects
• Autophagy/genetics
• Autophagy/physiology
• Autophagy-Related Protein 12
• Autophagy-Related Protein 5
• Base Sequence
• Cell Line, Tumor
• Gene Knockdown Techniques
• Humans
• Male
• Microtubule-Associated Proteins/antagonists & inhibitors
• Microtubule-Associated Proteins/genetics
• Microtubule-Associated Proteins/metabolism
• Prostatic Neoplasms/drug therapy
• Prostatic Neoplasms/genetics
• Prostatic Neoplasms/metabolism
• Prostatic Neoplasms/pathology
• RNA, Neoplasm/genetics
• RNA, Neoplasm/metabolism
• Sequestosome-1 Protein
• Small Ubiquitin-Related Modifier Proteins/metabolism
• Transfection
• Valproic Acid/pharmacology

• AVO
• BO-1051
• autophagy
• cell cycle
• checkpoint kinases

Conventional chemotherapeutic agents are often toxic not only to tumor cells but also to normal cells, limiting their therapeutic use in the clinic. Novel natural product anticancer compounds present an attractive alternative to synthetic compounds, based on their favorable safety and efficacy profiles. Several pre-clinical and clinical studies have demonstrated the anticancer potential of Panax ginseng, a widely used traditional Chinese medicine. The anti-tumor efficacy of ginseng is attributed mainly to the presence of saponins, known as ginsenosides. In this review, we focus on how ginsenosides exert their anticancer effects by modulation of diverse signaling pathways, including regulation of cell proliferation mediators (CDKs and cyclins), growth factors (c-myc, EGFR, and vascular endothelial growth factor), tumor suppressors (p53 and p21), oncogenes (MDM2), cell death mediators (Bcl-2, Bcl-xL, XIAP, caspases, and death receptors), inflammatory response molecules (NF-κB and COX-2), and protein kinases (JNK, Akt, and AMP-activated protein kinase). We also discuss the structure–activity relationship of various ginsenosides and their potentials in the treatment of various human cancers. In summary, recent advances in the discovery and evaluation of ginsenosides as cancer therapeutic agents support further pre-clinical and clinical development of these agents for the treatment of primary and metastatic tumors.

• Panax genus
• Panax ginseng
• anticancer activities
• clinical trials
• ginsenosides
• molecular mechanism
• pre-clinical pharmacology
• structure–activity relationship

• Apoptosis
• Cell cycle
• Chemoprevention
• Hepatocarcinogenesis
• Hepatocellular carcinoma
• Liver cancer cells
• Terpenoids
• Treatment