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The aim of this study was to reveal the novel roles of calmodulin 2 (CALM2) in hepatocellular carcinoma (HCC) progression.
The effects of knockdown of CALM2 expression by siRNA were investigated using various experimental approaches in both cellular and molecular levels.
Silencing of CALM2 inhibited HCC cell proliferation and colony formation through induction of apoptosis. At the molecular level, CALM2-specific knockdown led to the common dysregulation of 154 genes in HCC cells. Notably, E2F transcription factor 5 (E2F5), which is functionally associated with migration, invasion and proliferation, was generally down-regulated. These functional associations were confirmed in HCC clinical samples. Reflecting the molecular changes, CALM2 knockdown reduced the migration and invasion abilities of HCC cells and abrogated the potency of tumor formation in vivo.
Targeting CALM2 may be a molecular strategy for both primary HCC treatment and prevention of metastasis or recurrence.
Targeting CALM2 may be a molecular strategy for both primary HCC treatment and prevention of metastasis or recurrence.
Microsomal prostaglandin (PG) E synthase-1 (mPGES-1) is a terminal enzyme in PGE
synthesis and highly expressed in several cancers. In this study, to reveal the involvement of mPGES-1 in skin carcinogenesis, the effect of mPGES-1 deficiency on two-stage skin carcinogenesis in mice was investigated.
A two-stage skin carcinogenesis model using 7,12-dimethylbenz[a]anthracene (DMBA) as an initiator and 12-O-tetradecanoylphorbol-13-acetate (TPA) as a promoter was applied on mPGES-1 knockout (KO) mice and littermate wild-type mice of a Balb/c genetic background.
DMBA/TPA-induced skin carcinogenesis was suppressed in mPGES-1 KO mice. The induction of IL-17 and other inflammatory cytokines by TPA was also suppressed by mPGES-1 deficiency, although DMBA-induced apoptosis was not affected.
mPGES-1 promotes chemically induced skin carcinogenesis and might play an important role in the TPA-induced promotion phase of the two-stage skin carcinogenesis model. ACP-196 chemical structure mPGES-1 inhibition may be a therapeutic target for skin cancer.
mPGES-1 promotes chemically induced skin carcinogenesis and might play an important role in the TPA-induced promotion phase of the two-stage skin carcinogenesis model. mPGES-1 inhibition may be a therapeutic target for skin cancer.
A xanthophyll of fucoxanthin (Fx) is a potential chemopreventive agent. Familial adenomatous polyposis (FAP) is an inherited disease that is associated with a high risk of developing colorectal cancer. However, it remains unclear whether Fx can modify colorectal tumorigenesis in Apc
mice, a model mouse for human FAP.
We investigated the chemopreventive effect of Fx in dextran sodium sulfate (DSS)-treated Apc
mice.
Administration of Fx in the diet for 5 weeks significantly suppressed the number of colorectal adenocarcinomas in DSS-treated male Apc
mice, although the treatment did not affect the occurrence of colorectal dysplastic crypts and adenoma in the mice. In addition, Fx down-regulated cyclin D1 expression (0.6-fold) in colorectal mucosa of Apc
mice when compared with that of the control mice.
Fx possesses chemopreventive potential against progression of colorectal carcinogenesis in Apc
mice that receive inflammatory stimuli.
Fx possesses chemopreventive potential against progression of colorectal carcinogenesis in ApcMin/+ mice that receive inflammatory stimuli.
MALT type lymphoma belongs to marginal zone lymphoma (MZL). MALT lymphomas' inflammatory microenvironment contributes to the pathogenesis of this cancer. In this study, we analyzed and quantified the tumor inflammatory microenvironment in MALT lymphoma samples and in healthy controls, and the microvessel content by immunohistochemistry and morphometric estimation.
Biopsy specimens from MALT type lymphoma patients and from non-metastatic axillary lymph nodes (CTRL) were analyzed by immunochemistry in order to quantify CD3, CD4, CD8, CD68, CD163, tryptase, CD34, and Ki67 positive cells.
A substantial increase in the number of cells that were positive for the above markers and microvascular density (MVD) were observed in the MALT group. We also found a positive correlation between microvessels and CD8
cells and between CD8
cells and M2 type macrophages, while tryptase
mast cells correlated with CD4
cells. The mitotic proliferation index Ki67 was higher in MALT samples.
The interactions between inflammatory cells in the tumor microenvironment and their correlation with angiogenesis is a useful tool in the development of new immunotherapy strategies.
The interactions between inflammatory cells in the tumor microenvironment and their correlation with angiogenesis is a useful tool in the development of new immunotherapy strategies.
In previous work we showed that expression of heat-shock protein 27 (HSP27; encoded by HSPB1) was associated with inherent resistance to 5-fluorouracil (5-FU). However, the relationship between HSP27 and acquired resistance remains unknown.
We generated an acquired resistance model (WiDr-R) of a colon cancer cell line by exposing WiDr cells to 5-FU. Cell viability assays under treatment with 5-FU, as well as down-regulation of HSP27 using small interfering HSP27 RNA, were performed. HSP27 mRNA and protein expression was analyzed using real-time polymerase chain reaction and western blotting.
5-FU-acquired resistance induced overexpression of HSP27 mRNA and protein levels in WiDr-R cells. Furthermore, siRNA knockdown of HSP27 in WiDr-R cells reduced 5-FU-acquired resistance.
These findings demonstrate that HSP27 is associated with 5-FU resistance in human colon cancer cell cells and suggest that HSP27 regulation represents a novel approach to overcoming chemoresistance in colorectal cancer.
These findings demonstrate that HSP27 is associated with 5-FU resistance in human colon cancer cell cells and suggest that HSP27 regulation represents a novel approach to overcoming chemoresistance in colorectal cancer.
We aimed to investigate the synergistic effects of apigenin and curcumin on the cross-talk between apoptosis and autophagic cell death, as well as on paraptosis in HeLa cells.
Cell viability was measured using the MTT assay. Synergistic effects were measured using the Bliss independence model. qRT-PCR was used to study the expression of genes related to apoptosis, autophagic cell death, and cross-talk. GRP78/BiP immunostaining was used to identify endoplasmic reticulum (ER) stress.
Treatment with a combination of apigenin and curcumin increased the expression levels of genes related to cell death in HeLa cells 1.29- to 27.6-fold. The combination of curcumin and apigenin showed a synergistic anti-tumor effect via cross-talk between processes leading to apoptosis and autophagic cell death, as well as ER stress-associated paraptosis. GRP78 expression was down-regulated, and massive cytoplasmic vacuolization was observed in HeLa cells.
The combination of curcumin and apigenin is an effective potential therapeutic for cervical cancers.
