scholarly journals Downregulation of PITX2 inhibits the proliferation and migration of liver cancer cells and induces cell apoptosis

2021 ◽  
Vol 16 (1) ◽  
pp. 1322-1329
Author(s):  
Kebinuer Tuerxun ◽  
Shufang Zhang ◽  
Yuexin Zhang
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cancer Progression ◽  
Cell Apoptosis ◽  
Migration And Invasion ◽  
Liver Cancer Cell ◽  
Liver Cancer Cells ◽  
And Migration ◽  
Pitx2 Expression

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.

scholarly journals MiR-155 Inhibits Malignant Biological Behavior of Human Liver Cancer Cells by Regulating SRPK1

2021 ◽  
Vol 20 ◽  
pp. 153303382095702
Author(s):  
Qi Wang ◽  
Guo-tai Wang ◽  
Wei-hong Lu
Keyword(s):  
Cell Proliferation ◽  
Liver Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Migration And Invasion ◽  
Cancer Cell Proliferation ◽  
Liver Cancer Cell ◽  
Liver Cancer Cells ◽  
Proliferation And Metastasis ◽  
Cell Proliferation And Metastasis

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.

scholarly journals miR-18a-5p Targets FBP1 to Promote Proliferation, Migration, and Invasion of Liver Cancer Cells and Inhibit Cell Apoptosis

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Shan Gao ◽  
Dongjie Zhu ◽  
Jian Zhu ◽  
Lianqiang Shen ◽  
Ming Zhu ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Cell Apoptosis ◽  
Malignant Tumors ◽  
Luciferase Assay ◽  
Migration And Invasion ◽  
Cancer Tissue ◽  
Liver Cancer Cells ◽  
Treatment Plans ◽  
New Treatment

Liver cancer is one of the most aggressive malignant tumors. It is significant to understand the molecular mechanism of liver cancer cells to develop new treatment plans. Studies have identified that FBP1 serves as a cancer inhibitor gene. To research the effect mechanism of FBP1 in liver cancer cells, bioinformatics analysis was performed to study its expression in liver cancer tissue. Survival analysis was also performed. Moreover, starBase database was applied to predict upstream regulatory genes of FBP1. Dual-luciferase assay was performed to testify their targeted relationship. The mRNA and protein expression levels of FBP1 in liver cancer cells were detected by qRT-PCR and western blot, respectively. Cell viability was analyzed by CCK-8 assay. The migratory and invasive abilities of cells were analyzed by Transwell assay. The apoptosis of liver cancer cells was detected by flow cytometry. The results showed that the expression of FBP1 was downregulated in liver cancer tissue and cells. FBP1 low expression was correlated with the poor prognosis of patients. miR-18a-5p could inhibit FBP1 expression. Overexpression of FBP1 could inhibit the progression of liver cancer cells and promote cell apoptosis. Overexpressing miR-18a-5p could promote the progression of liver cancer cells and inhibit cell apoptosis. However, overexpressing FBP1 simultaneously could reverse the effect. miR-18a-5p and FBP1 are expected to be candidates for liver cancer treatment.

scholarly journals Mechanism of action of novel piperazine containing compound toxicant against human liver cancer cells

PeerJ ◽  
2016 ◽  
Vol 4 ◽  
pp. e1588 ◽  
Author(s):  
Nima Samie ◽  
Sekaran Muniandy ◽  
MS Kanthimathi ◽  
Batoul Sadat Haerian
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Cell Lines ◽  
Cancer Cell ◽  
Human Liver ◽  
Cancer Cell Lines ◽  
Liver Cancer Cell ◽  
Liver Cancer Cells ◽  
Human Liver Cancer ◽  
Human Liver Cancer Cells

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.

scholarly journals Novel piperazine core compound induces death in human liver cancer cells: possible pharmacological properties

2016 ◽  
Vol 6 (1) ◽  
Author(s):  
Nima Samie ◽  
Sekaran Muniandy ◽  
M. S. Kanthimathi ◽  
Batoul Sadat Haerian ◽  
Raja Elina Raja Azudin
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Cell Line ◽  
Cell Lines ◽  
Cancer Cell ◽  
Human Liver ◽  
Liver Cancer Cell ◽  
Liver Cancer Cells ◽  
Human Liver Cancer ◽  
Human Liver Cancer Cells

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.

scholarly journals Morphine Suppresses Liver Cancer Cell Tumor Properties In Vitro and In Vivo

2021 ◽  
Vol 11 ◽  
Author(s):  
Hao-Wen Zhang ◽  
Fei Wang ◽  
Ya-Qun Zhou ◽  
San-Ping Xu ◽  
Shi-Ying Yu ◽  
...  
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Hepg2 Cells ◽  
Cell Tumor ◽  
Liver Cancer Cell ◽  
Liver Cancer Cells ◽  
Sphere Formation

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.

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
Keyword(s):  
Liver Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Curcuma Longa ◽  
Hot Water ◽  
Liver Cancer Cell ◽  
Apoptosis Pathway ◽  
P53 Expression ◽  
Liver Cancer Cells ◽  
Protein Expressions

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.

scholarly journals Arf6-driven endocytic recycling of CD147 determines HCC malignant phenotypes

2019 ◽  
Vol 38 (1) ◽  
Author(s):  
Shanshan Qi ◽  
Linjia Su ◽  
Jing Li ◽  
Chuanshan Zhang ◽  
Zhe Ma ◽  
...  
Keyword(s):  
Cell Adhesion ◽  
Liver Cancer ◽  
Cancer Cells ◽  
Cancer Progression ◽  
Membrane Trafficking ◽  
Gelatin Zymography ◽  
Confocal Imaging ◽  
Migration And Invasion ◽  
Endocytic Recycling ◽  
Liver Cancer Cells

Abstract Background Adhesion molecules distributed on the cell-surface depends upon their dynamic trafficking that plays an important role during cancer progression. ADP-ribosylation factor 6 (Arf6) is a master regulator of membrane trafficking. CD147, a tumor-related adhesive protein, can promote the invasion of liver cancer. However, the role of Arf6 in CD147 trafficking and its contribution to liver cancer progression remain unclear. Methods Stable liver cancer cell lines with Arf6 silencing and over-expression were established. Confocal imaging, flow cytometry, biotinylation and endomembrane isolation were used to detect CD147 uptake and recycling. GST-pull down, gelatin zymography, immunofluorescence, cell adhesion, aggregation and tight junction formation, Transwell migration, and invasion assays were used to examine the cellular phenotypes. GEPIA bioinformatics, patient’s specimens and electronic records collection, and immunohistochemistry were performed to obtain the clinical relevance for Arf6-CD147 signaling. Results We found that the endocytic recycling of CD147 in liver cancer cells was controlled by Arf6 through concurrent Rab5 and Rab22 activation. Disruption of Arf6-mediated CD147 trafficking reduced the cell-matrix and cell-cell adhesion, weakened cell aggregation and junction stability, attenuated MMPs secretion and cytoskeleton reorganization, impaired HGF-stimulated Rac1 activation, and markedly decreased the migration and invasion of liver cancer cells. Moreover, high-expression of the Arf6-CD147 signaling components in HCC (hepatocellular carcinoma) was closely correlated with poor clinical outcome of patients. Conclusions Our results revealed that Arf6-mediated CD147 endocytic recycling is required for the malignant phenotypes of liver cancer. The Arf6-driven signaling machinery provides excellent biomarkers or therapeutic targets for the prevention of liver cancer.

scholarly journals Inhibition of human liver cancer cell growth by evodiamine involves apoptosis and deactivation of PI3K/AKT pathway

2020 ◽  
Vol 63 (1) ◽  
Author(s):  
Jia Jia ◽  
Xigang Kang ◽  
Yanfang Liu ◽  
Jianwei Zhang
Keyword(s):  
Liver Cancer ◽  
Cancer Cell ◽  
Human Liver ◽  
Akt Pathway ◽  
Migration And Invasion ◽  
Dependent Manner ◽  
Liver Cancer Cell ◽  
Human Liver Cancer Cell ◽  
Human Liver Cancer ◽  
Induction Of Apoptosis

Abstract Evodiamine is an active alkaloid member found in Traditional Chinese Herb (TCH) Evodia rutaecarpa. It has been reported to exhibit remarkable biological and medicinal activities including anticancer and anti-inflammatory. This study was designed to investigate the anticancer effects of evodiamine against human liver cancer and evaluate its effects on cell migration, cell invasion, cellular apoptosis and PI3K/AKT pathway. The results showed that evodiamine exhibits potent antiproliferative effects against two human liver cancer cell lines (HepG2 and PLHC-1) with an IC50 of 20 µM. Nonetheless, the cytotoxic effects of evodiamine were comparatively low against the normal cells as evident from the IC50 of 100 μM. The growth inhibitory effects of evodiamine were found to be due to the induction of apoptosis as revealed by the DAPI, AO/EB and annexin V/PI staining assays. The induction of apoptosis was also associated with upregulation of Bax and downregulation of Bcl-2 expression in a concentration dependent manner. The wound healing and transwell assay revealed that evodiamine caused a significant decline in the migration and invasion of the HepG2 and PLHC-1 cells. Investigation of the effects of evodiamine on the PI3K/AKT signalling revealed that evodiamine inhibited the phosphorylation of PI3K and AKT proteins. Taken together, the results showed that evodiamine inhibits the growth of human liver cancer via induction of apoptosis and deactivation of PI3K/AKT pathway. The results point towards the therapeutic potential of evodiamine in the treatment of liver cancer.

scholarly journals Circular RNA FLNA acts as a sponge of miR-486-3p in promoting lung cancer progression via regulating XRCC1 and CYP1A1

2021 ◽  
Author(s):  
Jiongwei Pan ◽  
Gang Huang ◽  
Zhangyong Yin ◽  
Xiaoping Cai ◽  
Enhui Gong ◽  
...  
Keyword(s):  
Lung Cancer ◽  
Cancer Cells ◽  
Cancer Cell ◽  
Cancer Progression ◽  
Lung Cancer Cells ◽  
Luciferase Reporter ◽  
Migration And Invasion ◽  
Related Factors

AbstractSignificantly high-expressed circFLNA has been found in various cancer cell lines, but not in lung cancer. Therefore, this study aimed to explore the role of circFLNA in the progression of lung cancer. The target gene of circFLNA was determined by bioinformatics and luciferase reporter assay. Viability, proliferation, migration, and invasion of the transfected cells were detected by CCK-8, colony formation, wound-healing, and transwell assays, respectively. A mouse subcutaneous xenotransplanted tumor model was established, and the expressions of circFLNA, miR-486-3p, XRCC1, CYP1A1, and related genes in the cancer cells and tissues were detected by RT-qPCR, Western blot, or immunohistochemistry. The current study found that miR-486-3p was low-expressed in lung cancer. MiR-486-3p, which has been found to target XRCC1 and CYP1A1, was regulated by circFLNA. CircFLNA was located in the cytoplasm and had a high expression in lung cancer cells. Cancer cell viability, proliferation, migration, and invasion were promoted by overexpressed circFLNA, XRCC1, and CYP1A1 but inhibited by miR-486-3p mimic and circFLNA knockdown. The weight of the xenotransplanted tumor was increased by circFLNA overexpression yet reduced by miR-486-3p mimic. Furthermore, miR-486-3p mimic reversed the effect of circFLNA overexpression on promoting lung cancer cells and tumors and regulating the expressions of miR-486-3p, XRCC1, CYP1A1, and metastasis/apoptosis/proliferation-related factors. However, overexpressed XRCC1 and CYP1A1 reversed the inhibitory effect of miR-486-3p mimic on cancer cells and tumors. In conclusion, circFLNA acted as a sponge of miR-486-3p to promote the proliferation, migration, and invasion of lung cancer cells in vitro and in vivo by regulating XRCC1 and CYP1A1.

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