Explore positive published findings by substance, cancer biology, treatment interaction and quality-of-life outcome.
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Browse 27 source-linked studies with the full title, publication year, research focus and a concise finding. Select any linked substance to move directly to its corresponding Sunridge page.
Network calculation and a series of in vivo and in vitro experimental data demonstrated that the apoptosis-related GBA-ceramide-CTSD-BID-BAX signaling was one of the key putative target pathways by which artesunate may inhibit the malignant progression of HCC.
Our results demonstrated that artesunate significantly inhibited HCC cell viability, migration, and invasion.
Mechanically, artesunate reduced the expression of AFAP1L2 protein, suppressed the phosphorylation levels of SRC and FUNDC1 proteins, promoted the FUNDC1 recruitment of massive LC3B to mitochondria, and further overactivated the mitophagy and subsequent cell apoptosis of sorafenib resistant cells.
We showed that artesunate greatly enhanced the anticancer effects of low dose of sorafenib against Huh7, SNU-449, and SNU-182 HCC cell lines in vitro and against Huh7 cell xenograft model in Balb/c nude mice.
Our previous research showed that dihydroartemisinin (DHA) inhibited cell proliferation in HepG2 and HepG22215 cells.
As demonstrated from our results, we found berberine greatly enhanced the inhibitory effects of sorafenib on cell proliferation synergistically against mouse and human liver cancer cell lines in vitro, Hepa1-6 xenograft model in C57/B6J mice in vivo and in the 3D culture system of tumor cells.
Therefore, curcumin exerts anti-cancer effects by inhibiting cell proliferation and promoting cell apoptosis in HCC.
Curcumin administration (100 mg/kg for 15 days) markedly suppressed tumor growth, reduced glutathione levels in tumor tissues, and enhanced the accumulation of reactive oxygen species, malondialdehyde, and Fe2+.In vitro, curcumin inhibited HepG2 cell proliferation, promoted ferroptotic cell death, downregulated P62 and NRF2 expression, and upregulated KEAP1 expression.
Curcumin (CUR) as one of the natural edible pigments is approved by the World Health Organization due to its nontoxic and anticancer effect.
EGCG significantly reduced cell proliferation and induced apoptosis in all cell lines.
Ginsenoside Rh2 (Rh2) and luteolin (Lut) each exhibits anticancer activity; however, their behavior in combination and underlying mechanisms in HCC remain largely unexplored.
Here we investigate whether ginsenoside Rh3, a bioactive constituent of Panax ginseng, enhances the anticancer properties of regorafenib, a multikinase inhibitor, in hepatocellular carcinoma (HCC).
The elevated migration and invasion of HCC cells triggered by LPS were reduced by Rh4.
Importantly, co-treatment of ginsenoside Rk1 with autophagy inhibitors can inhibit apoptosis of HCC cells, once again demonstrating the ability of ginsenoside Rk1 to promote autophagy-dependent apoptosis.
Various inhibitors targeting apoptosis (Z-VAD-FMK 20 μM), necrosis (Nec-1, 10 μM), and ferroptosis (Fer-1, 10 μM; Lip-1, 1 μM) were employed to assess ginsenoside RK1's impact on cell demise.
Ginsenoside Rh2 (Rh2) is one of the main bioactive ginsenosides that act as a natural antitumor drug.
We demonstrated that ivermectin at clinically relevant concentrations was active against growth and survival in multiple HCC cell lines.
A decrease in secondary bile acids along with changes in gut microbiota were observed.
However, the role of the microbiome in regulating the response to RT remains unclear.
We observed that taxa abundance in HCC tissues was significantly associated with clinicopathological variables, such as tumor size, differentiation, invasion of the liver capsule, lymphovascular invasion, metastasis, pTNM, portal hypertension (PTH), Child-Turcotte-Pugh score, BCLC stage, prognosis (overall survival and progression-free survival), serum levels of α-fetoprotein, albumin, and glucose and personal habits (such as smoking and alcohol intake) of the HBV-associated HCC patients (p < 0.05).
In vivo, quercetin reduced VEGF secretion, impaired angiogenesis, slowed tumor growth, and decreased the number and proportion of VEGFR2-positive CTCs.
We explored whether quercetin could inhibit cell migration or invasion by transwell assay.
Therefore, we designed a clinical trial to test whether sirolimus can improve recurrence-free survival (RFS) in hepatocellular carcinoma (HCC) patients beyond the Milan criteria after LT.
The resveratrol was shown to suppress the proliferation of MCF-7 and HepG2 cells at dose- and time-dependent.
In our previous studies, 3-O-β-D-galactosylated resveratrol (Gal-Res) was synthesized by structural modification and then 3-O-β-D-galactosylated resveratrol polydopamine nanoparticles (Gal-Res NPs) were successfully prepared to improve the bioavailability and liver distribution of Res.
Inhibition of AMPK using small interfering RNA (siRNA) or compound C, an AMPK inhibitor, significantly attenuated the upregulation of DR5 and the apoptotic response induced by silibinin.
Vitamin C (L-ascorbic acid, ascorbate, VC) is an important natural antioxidant, which has been reported to show suppressive effects in cancer treatment.
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