In situ condensation of an anti-cancer drug into fibrin gel enabling effective inhibition of tumor cell growth

2019 ◽  
Vol 55 (78) ◽  
pp. 11679-11682 ◽  
Author(s):  
Masayasu Kuwahara ◽  
Hiroto Fujita ◽  
Yuka Kataoka ◽  
Yasuyo Nakajima ◽  
Masanobu Yamada ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Growth ◽  
Tumor Cell ◽  
Cancer Drug ◽  
Tumor Cell Growth ◽  
Fibrin Gel ◽  
Anti Cancer ◽  
Effective Inhibition

Efficient anti-cancer drug condensation enabled equally inhibiting cell proliferation even at a concentration of 7.6 ± 0.36 nM, which was approximately 170-fold lower than the standard therapeutic concentrations of camptothecin (CPT) drugs.

Advances in the 1-phenanthryl-tetrahydroisoquinoline series of PAK4 inhibitors: potent agents restrain tumor cell growth and invasion

2016 ◽  
Vol 14 (32) ◽  
pp. 7676-7690 ◽  
Author(s):  
Chenzhou Hao ◽  
Xiaodong Li ◽  
Shuai Song ◽  
Bingyu Guo ◽  
Jing Guo ◽  
...  
Keyword(s):  
Cell Growth ◽  
Tumor Cell ◽  
Natural Product ◽  
Tumor Cell Growth ◽  
New Class ◽  
Anti Cancer

Discovery of a new class of natural product-inspired PAK4 inhibitors as potent anti-cancer agents.

Vitronetcin promotes cell growth and inhibits apoptotic stimuli in a human hepatoma cell line via the activation of caspases

2014 ◽  
Vol 92 (5) ◽  
pp. 363-368 ◽  
Author(s):  
Wei Zhu ◽  
Yingzhi Liu ◽  
Konghe Hu ◽  
Wenxue Li ◽  
Jianling Chen ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Growth ◽  
Tumor Cell ◽  
Hepatoma Cell ◽  
Hepatoma Cells ◽  
Signaling Molecules ◽  
Hepatoma Cell Line ◽  
Dependent Manner ◽  
Tumor Cell Growth ◽  
Induced Apoptosis

This study sought to understand the effects of vitronectin (VTN) on the growth of SMMC-7721 hepatoma cells. In addition, this study examined how VTN inhibits the induction of apoptosis in SMMC-7721 cells by 3,3′-diindolylmethane (DIM), a metabolite of natural phytochemicals, and preliminarily investigated the signaling molecules involved in this process. A cell proliferation reagent was used to observe the effects of VTN on cell proliferation rates. Laser scanning confocal microscopy was performed to observe the effects of VTN on the morphology of tubulin, a component of the cytoskeleton. Flow cytometry and Western blotting assays were used to observe the inhibitory effects of VTN on DIM-induced apoptosis in SMMC-7721 cells and changes in the expression levels of the signaling molecules involved in this process. VTN promoted tumor cell growth in a concentration-dependent manner and inhibited apoptosis caused by the effects of apoptosis-inducing agents. Under in vitro experimental conditions, VTN contributed to the growth of SMMC-7721 hepatoma cells and protected them from the effects of an apoptosis-inducing agent. These findings suggest that during hepatocellular carcinogenesis, VTN may promote tumor cell growth and inhibit chemically induced apoptosis.

scholarly journals Trichinella spiralis ESP inhibits tumor cell growth by regulating the immune response and inducing apoptosis

2021 ◽  
Author(s):  
Jing Ding ◽  
Xiaolei Liu ◽  
Bin Tang ◽  
Xue Bai ◽  
Yang Wang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Growth ◽  
Tumor Cell ◽  
Trichinella Spiralis ◽  
Tumor Model ◽  
Cell Counting ◽  
Enzyme Linked Immunosorbent Assay ◽  
Secretory Product ◽  
Tumor Cell Growth ◽  
Th1 Cytokines

Abstract Background Although Trichinella spiralis (T. spiralis) causes zoonotic diseases, it has a strong immunomodulatory effect and has therapeutic potential for various autoimmune diseases and cancers. Our previous study results showed that T. spiralis infection can inhibit the growth of liver cancer cells, but the specific mechanism has not been elucidated. Methods BALB/c mice injected with H22 cells and then infected with T. spiralis were used to detect tumor inhibition rate. Cell proliferation and apoptosis of H22 cells treated with excretory-secretory product (ESP) were measured by Cell-Counting Kit 8 (CCK-8) and Flow Cytometry (FCM). The expression of apoptosis-related genes in H22 cells and tumor tissues was detected by western blotting and real-time quantitative PCR (qPCR). IL-2, IFN-γ and IL-4 production in the spleens were measured by qPCR and enzyme-linked immunosorbent assay(ELISA). Results The growth of tumors in tumor model mice infected with T. spiralis was significantly inhibited compared with those uninfected tumor model mice. ESP could inhibit H22 cell proliferation and induce apoptosis through the mitochondrial pathway both in vitro and in vivo. Additionally, the levels of Th1 cytokines with antitumor effects were significantly increased in the early stage of T. spiralis infection, while Th2 cytokines increased later than Th1 cytokines. Conclusions ESP can directly induce tumor cell apoptosis and indirectly inhibit tumor cell growth through the host immune system, which is the potential antitumor mechanism of T. spiralis infection.

Effects of Selaginella tamariscina on in vitro tumor cell growth, p53 expression, G1 arrest and in vivo gastric cell proliferation

1999 ◽  
Vol 144 (1) ◽  
pp. 93-99 ◽  
Author(s):  
In-Seon Lee ◽  
Akiyoshi Nishikawa ◽  
Fumio Furukawa ◽  
Ken-ichiro Kasahara ◽  
Soo-Un Kim
Keyword(s):  
Cell Proliferation ◽  
Cell Growth ◽  
Tumor Cell ◽  
G1 Arrest ◽  
Tumor Cell Growth ◽  
P53 Expression ◽  
Gastric Cell ◽  
Selaginella Tamariscina

scholarly journals SKA3 Promotes Cell Growth in Breast Cancer by Inhibiting PLK-1 Protein Degradation

2020 ◽  
Vol 19 ◽  
pp. 153303382094748
Author(s):  
Li-wei Ruan ◽  
Peng-peng Li ◽  
Lang-ping Jin
Keyword(s):  
Breast Cancer ◽  
Cervical Cancer ◽  
Cell Proliferation ◽  
Cell Growth ◽  
Cell Lines ◽  
Cancer Progression ◽  
Cancer Drug ◽  
Anti Cancer ◽  
Mental And Physical Health

Breast cancer (Bca) remains the most common form of malignancy affecting females in China, leading to significant reductions in the mental and physical health of those with this condition. While spindle and kinetochore associated complex subunit 3 (SKA3) is known to be linked with cervical cancer progression, whether it is similarly associated with Bca progression remains unknown. Using shRNA, we specifically knocked down the expression of SKA3 in Bca cell lines and then assessed the resultant changes in cell proliferation using CCK-8 and colony formation assays. In addition, we used western blotting to quantify the expression levels of relevant proteins in these cells, and we assessed the interaction between SKA3 and polo-like kinase-1 (PLK-1) via co-immunoprecipitation.In this study, we observed elevated SKA3 expression in Bca tissues and cell lines. When we knocked down SKA3 expression in Bca cells, we were able to determine that it functions in an oncogenic manner so as to promote the growth and proliferation of these cells in vitro. From a mechanistic perspective, we were able to show that in Bca cells SKA functions at least in part via interacting with PLK-1 and preventing its degradation. In summary, we found that SKA3 is able to regulate PLK-1 degradation in Bca cells, thus controlling their growth and proliferation. These results highlight SKA3 as a potentially viable target for anti-cancer drug development aimed at combatting Bca.

scholarly journals Depleting RhoA/Stress Fiber-Organized Fibronectin Matrices on Tumor Cells Non-Autonomously Aggravates Fibroblast-Driven Tumor Cell Growth

2020 ◽  
Vol 21 (21) ◽  
pp. 8272
Author(s):  
Li-Tzu Huang ◽  
Chen-Lung Tsai ◽  
Shin-Huei Huang ◽  
Ming-Min Chang ◽  
Wen-Tsan Chang ◽  
...  
Keyword(s):  
Cell Proliferation ◽  
Cell Growth ◽  
Tumor Growth ◽  
Tumor Cell ◽  
Tumor Cells ◽  
Stress Fiber ◽  
Tumor Cell Growth ◽  
Primary Tumor Growth

Fibronectin (FN) expressed by tumor cells has been known to be tumor suppressive but the pericellular FN (periFN) assembled on circulating tumor cells appears to evidently promote distant metastasis. Whereas the regulation of periFN assembly in suspended cells has currently been under investigation, how it is regulated in adherent tumor cells and the role of periFN in primary tumor growth remain elusive. Techniques of RNAi, plasmid transfections, immunoblotting, fluorescence/immunohistochemistry staining, cell proliferation assays, and primary tumor growth in C57BL6 mice and Fischer 344 rats were employed in this study. We found that endogenously synthesized FN in adherent tumor cells was required for periFN assembly which was aligned by RhoA-organized actin stress fiber (SF). Depleting periFN on adherent tumor cells congruently promoted in vivo tumor growth but surprisingly did not autonomously impact on in vitro tumor cell proliferation and apoptosis, suggestive of a non-autonomous role of periFN in in vivo tumor growth. We showed that the proliferative ability of shFN-expressing tumor cells was higher than shScramble cells did in the presence of fibroblasts. Altogether, these results suggested that depriving RhoA/SF-regulated periFN matrices non-autonomously promotes fibroblast-mediated tumor cell growth.

scholarly journals Extract Derived from Cedrus atlantica Acts as an Antitumor Agent on Hepatocellular Carcinoma Growth In Vitro and In Vivo

Molecules ◽  
2020 ◽  
Vol 25 (20) ◽  
pp. 4608 ◽  
Author(s):  
Xiao-Fan Huang ◽  
Kai-Fu Chang ◽  
Shan-Chih Lee ◽  
Gwo-Tarng Sheu ◽  
Chia-Yu Li ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Growth ◽  
Tumor Cell ◽  
Dependent Manner ◽  
Tumor Cell Growth ◽  
Normal Cells ◽  
Cedrus Atlantica ◽  
Anti Cancer

Cedrus atlantica is widely used in herbal medicine. However, the anti-cancer activity of C. atlantica extract (CAt extract) has not been clarified in hepatocellular carcinoma. In the study, we elucidated the anti-hepatoma capacity of CAt extract on HCC in vitro and in vivo. To explore the anti-hepatoma mechanisms of the CAt extract in vitro, HCC and normal cells were treated with the CAt extract, which showed marked inhibitory effects on HCC cells in a dose-dependent manner; in contrast, the CAt extract treatment was less cytotoxic to normal cells. In addition, our results indicate that the CAt extract induced apoptosis via caspase-dependent and independent apoptosis pathways. Furthermore, the CAt extract inhibited HCC tumor cell growth by restraining cell cycle progression, and it reduced the signaling of the AKT, ERK1/2, and p38 pathways. In the xenograft model, the CAt extract suppressed HCC tumor cell growth and prolonged lifespan by inhibiting PCNA protein expression, repressing part of the VEGF-induced autocrine pathway, and triggering strong expression of cleaved caspase-3, which contributed to cell apoptosis. Moreover, the CAt extract did not induce any obvious changes in pathological morphology or body weight, suggesting it had no toxicity. CAt extract exerted anti-tumor effects on HCC in vitro and in vivo. Thus, CAt extract could be used as a potential anti-cancer therapeutic agent against HCC.

scholarly journals Influence of miR-520e-mediated MAPK signaling pathway on HBV replication and regulation of hepatocellular carcinoma cells via targeting EphA2

2018 ◽  
Author(s):  
Jing-hui Tian ◽  
Wen-dong Liu ◽  
Zhi-yong Zhang ◽  
Li-hua Tang ◽  
Dong Li ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Cell Proliferation ◽  
Cell Growth ◽  
Tumor Cell ◽  
Infected Mouse ◽  
Dna Content ◽  
Hbv Dna ◽  
Tumor Cell Growth ◽  
Hbv Replication ◽  
Mapk Pathways

AbstractThis paper aims to determine the role of miR-520e in the replication of hepatitis B virus (HBV) and the growth of hepatocellular carcinoma (HCC) cells. MiR-520e and EphA2 in HBV-positive HCC tissues and cells were detected. HepG2.2.15 and Huh7 cells transfected with pHBV1.2 were divided into Mock, NC, miR-520e mimic, miR-520e inhibitor, si-EphA2, and miR-520e inhibitor + si-EphA2 groups. MiR-520e, HBV DNA content, HBsAg and HBeAg levels, cell proliferation, apoptosis and protein expression of EphA2 and MAPK pathways were evaluated. Furthermore, rAAV81.3HBV infected-mouse model was established to detect HBV-DNA levels. MiR-520e was up-regulated and EphA2 was down-regulated in HBV-positive HCC tissues and cells (HepG2.2.15 and HepAD38). MiR-520e was decreased in Huh7-X and HepG2-X cells in which HBx was stably expressed, but miR-520e was dose-dependently elevated in Huh7-X, HepG2-X, and HepG2.2.15 cells after interfering HBx. Additionally, miR-520e mimic and si-EphA2 groups were apparently reduced in HBV DNA content, HBsAg and HBeAg levels, cell proliferation, and were enhanced in the expressions of EphA2, MAPK pathways and cell apoptosis. Furthermore, si-EphA2 can reverse the promotion effect of miR-520e inhibitor on the HBV replication and tumor cell growth Up-regulating miR-520e in rAAV81.3HBV infected-mouse resulted in the reduced EphA2 in liver tissues and HBV DNA content in serum. MiR-520e was found to be decreased in HBV-positive HCC tissues and cells, while over-expression of miR-520e blocked MAPK pathways via inhibiting EphA2, ultimately reducing HBV replication and inhibiting tumor cell growth.

Sign in / Sign up

Export Citation Format

Share Document