Combined Curcuma longa and Cratoxylum formosum Extracts Possess Anti-liver Cancer and Anti-HBV Activities in HepG2.2.15

2020 ◽  
Vol 06 ◽  
Author(s):  
Damita Jevapatarakul ◽  
Nattanan Panjaworayan T-Thienprasert ◽  
Sunchai Payungporn

Background: Curcuma longa Linn. and Cratoxylum formosum have been consumed as the Thai traditional medicine for curing liver diseases. However, biological effects from a combination of C. longa and C. formosum have not been investigated. Objective: This study focused to investigate effects of combined extracts on anti-liver cancer activity, anti-Hepatitis B virus (HBV) activity and alteration of miRNA expression including their effects on p53 and NF-κB protein expressions. Method: The cytotoxicity effects of hot water extract on liver cancer cells were examined by using MTT assay. Annexin V assay and Western blot analysis were conducted to investigate the effects of plant extracts on apoptosis pathway and cellular protein expressions. Finally, the expression of HBV genes and miRNA expressions were evaluated by using a quantitative real-time PCR. ResultS: The cell viability assay indicated that 400 µg/mL of combined C. longa and C. formosum extracts significantly inhibited different liver cancer cell lines without affecting a normal cell (Vero). The combined extracts could induce liver cancer cell death via apoptosis pathway by up-regulating p53 expression while down-regulating NF-κB expression. Moreover, 150 µg/mL of the combined extract specifically suppressed HBx gene expression in liver cancer cells that stably express HBV proteins. However, 150 µg/mL of the combined extract had no effect on miR-34a and miR-199a/b expressions. Conclusion: This study firstly reported anti-liver cancer and anti-HBV activities of the combined C. longa and C. formosum extracts.

PeerJ ◽  
2016 ◽  
Vol 4 ◽  
pp. e1588 ◽  
Author(s):  
Nima Samie ◽  
Sekaran Muniandy ◽  
MS Kanthimathi ◽  
Batoul Sadat Haerian

The purpose of this study was to assess the cytotoxic potential of a novel piperazine derivative (PCC) against human liver cancer cells. SNU-475 and 423 human liver cancer cell lines were used to determine the IC50 of PCC using the standard MTT assay. PCC displayed a strong suppressive effect on liver cancer cells with an IC50 value of 6.98 ± 0.11 µM and 7.76 ± 0.45 µM against SNU-475 and SNU-423 respectively after 24 h of treatment. Significant dipping in the mitochondrial membrane potential and elevation in the released of cytochrome c from the mitochondria indicated the induction of the intrinsic apoptosis pathway by PCC. Activation of this pathway was further evidenced by significant activation of caspase 3/7 and 9. PCC was also shown to activate the extrinsic pathways of apoptosis via activation of caspase-8 which is linked to the suppression of NF-κB translocation to the nucleus. Cell cycle arrest in the G1 phase was confirmed by flow cytometry and up-regulation of glutathione reductase expression was quantified by qPCR. Results of this study suggest that PCC is a potent anti-cancer agent inducing both intrinsic and extrinsic pathways of apoptosis in liver cancer cell lines.


2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Nima Samie ◽  
Sekaran Muniandy ◽  
M. S. Kanthimathi ◽  
Batoul Sadat Haerian ◽  
Raja Elina Raja Azudin

Abstract The current study evaluates the cytotoxic mechanism of a novel piperazine derivate designated as PCC against human liver cancer cells. In this context, human liver cancer cell lines, SNU-475 and 243, human monocyte/macrophage cell line, CRL-9855, and human B lymphocyte cell line, CCL-156, were used to determine the IC50 of PCC using the standard MTT assay. PCC displayed a strong suppressive effect on SNU-475 and SNU-423 cells with an IC50 value of 6.98 ± 0.11 μg/ml and 7.76 ± 0.45 μg/ml respectively, after 24 h of treatment. Significant dipping in the mitochondrial membrane potential and elevation in the released of cytochrome c from the mitochondria indicated the induction of the intrinsic apoptosis pathway by PCC. Activation of this pathway was further evidenced by significant activation of caspase 3/7 and 9. PCC was also shown to activate the extrinsic pathways of apoptosis via activation of caspase-8 which is linked to the suppression of NF-ƙB translocation to the nucleus. Cell cycle arrest in the G1 phase was confirmed by flow cytometry and up-regulation of glutathione reductase expression was quantified by qPCR. This study suggests that PCC is a simultaneous inducer of intrinsic and extrinsic pathways of apoptosis in liver cancer cell lines.


2021 ◽  
Vol 11 ◽  
Author(s):  
Hao-Wen Zhang ◽  
Fei Wang ◽  
Ya-Qun Zhou ◽  
San-Ping Xu ◽  
Shi-Ying Yu ◽  
...  

Morphine is an analgesic widely adopted to relieve cancer pain. A number of discrepancies, however, are presented by the published literature, with reports suggesting that opioids may either promote or inhibit the spread of cancer. It is of great significance to determine whether morphine may increase the risk of metastasis while utilized in liver cancer surgical treatment. In this study, we explore the effects of morphine on liver cancer cells in vitro and in vivo. Our results showed that morphine does not promote proliferative ability to cultured liver cancer cells. While morphine could increase the apoptosis rate of Hep3B/HepG2 cells. Furthermore, morphine could significantly inhibit the migratory and invasion ability of Hep3B/HepG2 cells. Subsequent investigations disclosed that morphine could inhibit sphere formation ability of Hep3B/HepG2 cells by using sphere formation assay. Based on nude mouse models, we demonstrated that morphine significantly reduced pulmonary tumorigenicity of Hep3B/HepG2 cells. In conclusion, our results found that morphine at clinical concentrations could suppress liver cancer cell tumor properties in vitro and in vivo, indicating the safety of morphine utilization in HCC patients’ pain management.


2021 ◽  
Vol 16 (1) ◽  
pp. 1322-1329
Author(s):  
Kebinuer Tuerxun ◽  
Shufang Zhang ◽  
Yuexin Zhang

Abstract Paired-like homeodomain 2 (PITX2) functions as a transcription factor to participate in vertebrate embryogenesis, and dysregulated PITX2 expression was associated with the progression of various cancers. The functional role of PITX2 in tumorigenesis of liver cancer remains unknown. Western blot analysis showed that expression levels of PITX2 were enhanced in the liver cancer tissues and cells. siRNAs targeting PITX2 induced downregulation of PITX2 in liver cancer cells. siRNA-induced knockdown of PITX2 decreased liver cancer cell viability and proliferation, while promoting cell apoptosis by increasing cleaved-PARP, cleaved caspase 3, and cleaved caspase 9. The knockdown of PITX2 repressed liver cancer cell migration and invasion. In conclusion, elevated PITX2 expression was associated with liver cancer progression through repression of cell apoptosis and promoting cell proliferation and metastasis, and silencing of PITX2 might serve as a potential therapeutic strategy for the treatment of liver cancer.


2021 ◽  
Vol 20 ◽  
pp. 153303382095702
Author(s):  
Qi Wang ◽  
Guo-tai Wang ◽  
Wei-hong Lu

Although the treatment of liver cancer has made great progress, the mechanism of its occurrence is not completely clear. miR-155 plays an important regulatory role in tumorigenesis and development, including survival, proliferation, migration and invasion. However, the role and regulatory mechanism of miR-155 in liver cancer has rarely been reported. We analyzed miR-155 expression in liver cancer tissue samples and cell lines by qRT-PCR. The expression of miR-155 was measured by qRT-PCR before and after miR-155-mimic and sh-miR-155 transfection. CCK-8 and clonogenic assays were used to detect the proliferation of liver cancer cells. Cell scratch and invasion assays were used to detect migration and invasion. RNA-seq was used to detect the difference in RNA expression in liver cancer cells. SRPK1 expression was detected in liver cancer cells before and after transfection by qRT-PCR and western blotting. We observed that miR-155 was downregulated in liver cancer tissues compared with normal tissues. Furthermore, we demonstrated that liver cancer cell proliferation, migration and invasion are markedly suppressed by miR-155. Importantly, we also demonstrated that SRPK1 is directly regulated by miR-155 during the process of liver cancer cell proliferation and metastasis. Finally, the overexpression of miR-155 inhibits malignant biological behavior of human liver cancer cells. We report the abnormal expression of the miR-155 cluster in liver cancer cells, which inhibits cancer cell proliferation and metastasis. In addition, we identified SRPK1 as a target gene of miR-155 during the process of liver cancer cell proliferation and metastasis.


Author(s):  
Siti Zubaidah Abdullah ◽  
Chean Ring Leong ◽  
Woei Yenn Tong ◽  
Jyh Chyang Pang ◽  
Wen-Nee Tan ◽  
...  

In this communication, anthocyanin-loaded dextran nanoparticles from Clitoria ternatea was synthesized and characterized to test its anti-proliferative activity on the human HepG2 liver cancer cell lines. By using dextran as an encapsulant polymer, the nanoparticles appeared to be spherical, with an average size of 45.5 ± 11 nm. The surface charge of the anthocyanin-loaded dextran nanoparticle was -4.39 mV, which slightly relative to free anthocyanin (-4.46 mV), which indicate good dispersion stabilities. The Fourier transform infrared analysis showed that the anthocyanins from C. ternatea was successfully encapsulated in dextran nanoparticles. Overall, the percentage of drug encapsulation efficiency was 3.03%. Based on the stability test, the anthocyanin-loaded dextran nanoparticle showed significantly better color stability index compared to free anthocyanin, particularly at the presence of light and temperature of 37°C and 50°C. In the anti-proliferation assay on HepG2 liver cancer cell lines, the viability of the cancer cells was significantly reduced after treatment with the anthocyanin-loaded dextran nanoparticle. The anti-proliferation activities of the nanoparticles were significantly better than free anthocyanin. Our findings revealed the ability of the anthocyanin-loaded dextran nanoparticle, in particular from C. ternatea, as an effective anti-proliferative agent against cancer cells. Nanoencapsulation with dextran significantly improve the efficacy and stability of the anthocyanins. Further investigations should be done to evaluate the in vivo efficacy.


2022 ◽  
Vol 12 (2) ◽  
pp. 323-328
Author(s):  
Hao Cai ◽  
Jian Du ◽  
Cheng Luo

We aimed to explore whether microRNA (miRNA)-136-5p modulates P53 expression, and affects the efficacy of docetaxel treatment for liver cancer. miRNA array screened the differentially expressed miRNAs in biopsy tissues of liver cancer patients, and the expression of miR-136-5p and P53 in tissues and cells by RT-PCR. Following docetaxel treatment, through increased- and decreased-function method, we detected the impact of the miRNA on cell progression, as well as the sensitivity of docetaxel through MTT assay and colony formation experiment. The correlation between miR-136-5p and P53 was evaluated. The expression of miR-136-5p in liver cancer cells is up-regulated, which is consistent with the results of bioinformatics analysis. Further, miR-136-5p overexpression promoted cell proliferation and migration, and sensitized liver cancer cells to docetaxel. Interestingly, P53 was indicated to bind to miR-136-5p, and P53 participated in the up-regulation of MMP10 induced by miR-136-5p. miR-136-5p enhances the sensitivity to docetaxel in liver cancer and thus could be a biomarker for the treatment against liver cancer.


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