The TBX1/miR-193a-3p/TGF-2 Axis Mediates CHD by Promoting Ferroptosis.

Congenital heart disease (CHD) is the most common noninfectious cause of death during the neonatal stage. T-box transcription factor 1 (TBX1) is the main genetic determinant of 22q11.2 deletion syndrome (22q11.

GDF15 knockdown promotes erastin-induced ferroptosis by decreasing SLC7A11 expression.

Ferroptosis is an iron-dependent form of regulated cell death. GDF15 affects various properties of cancer cells, but the role of GDF15 in ferroptosis has not been reported. In the present study, we found that GDF15 knockdown led to decreased expression of SLC7A11, which is a key component of system X and a regulator of ferroptosis, indicating that GDF15 might play important roles in ferroptosis.

MicroRNA-375 inhibits the proliferation, migration and invasion of kidney cancer cells by triggering apoptosis and modulation of PDK1 expression.

Kidney cancer is one of the deadly cancers and is the cause of significant number of deaths worldwide. The treatments used for the treatment of kidney cancer are limited and associated with number of side effects. Therefore, there is need for the development of new drug options or to identify novel therapeutic targets for the treatment of kidney cancer.

Valsartan prevents glycerol-induced acute kidney injury in male albino rats by downregulating TLR4 and NF-κB expression.

In this study, the protective effect of valsartan against glycerol-induced acute kidney injury (AKI) in male albino rats was investigated. Valsartan is used to treat high blood pressure and congestive heart failure and can prolong lifespan following a heart attack. The rats were divided into control, AKI, AKI + valsartan 100 mg/kg bw, and AKI + valsartan 200 mg/kg bw groups.

IL-1β promotes the nuclear translocaiton of S100A4 protein in gastric cancer cells MGC803 and the cell's stem-like properties through PI3K pathway.

It has been shown that nuclear expression of S100A4 is significantly correlated with increased metastasis and reduced survival in patients with gastric cancer and many other cancers. However, the factors which could influence the nuclear contents of S100A4 in cancer cells are not clear. It has also been reported that Interleukin-1β (IL-1β) promotes the nuclear translocation of S100A4 in chondrocytes.

miR-3189-3p Mimics Enhance the Effects of S100A4 siRNA on the Inhibition of Proliferation and Migration of Gastric Cancer Cells by Targeting CFL2.

is a downstream gene of . miR-3189 is embedded in the intron of -and coexpressed with it. miR-3189-3p functions to inhibit the proliferation and migration of glioblastoma cells.

FAM107B is regulated by S100A4 and mediates the effect of S100A4 on the proliferation and migration of MGC803 gastric cancer cells.

FAM107B expression was decreased in stomach cancer and many other kinds of cancer. The forced expression of FAM107B in HeLa cells diminished proliferation in response to growth factors, suggesting that FAM107B might play important roles in many types of cancers. But the mechanisms underlying the decreased expression of FAM107B in cancers are not clear, the functional significance needs to be further clarified.

S100A4 influences cancer stem cell-like properties of MGC803 gastric cancer cells by regulating GDF15 expression.

Many studies have revealed that S100A4 is involved in cancer progression by affecting a variety of biological functions. Our previous study showed that S100A4 influences many biological properties of gastric cancer cells; however, the underlying mechanisms are far from clear. In this study, we used cDNA microarray analysis to investigate the global alterations in gene expression in MGC803 gastric cancer cells after siRNA-mediated S100A4 inhibition.

RNA interference-mediated silencing of speckle-type POZ protein promotes apoptosis of renal cell cancer cells.

This study aimed to investigate the effects of silencing the speckle-type POZ protein (SPOP) gene on renal cell cancer (RCC) cells and to explore its possible mechanism. The A498 and ACHN RCC cells were transfected with small interference RNA (siRNA)-SPOP by lipofection methods. The silencing efficiency was monitored by quantitative real-time polymerase chain reaction and Western blot.

EZH2 Mediates the Regulation of S100A4 on E-cadherin Expression and the Proliferation, Migration of Gastric Cancer Cells.

Background/aims: Several reports have showed the inverse correlation between S100A4 and E-cadherin expression, but the exact molecular mechanism remained unclear. It has been reported that EZH2 mediates transcriptional silencing of E-cadherin by trimethylating lysine 27 of histone H3 (H3K27me3). Therefore, we hypothesized that EZH2 might mediate the inhibition of S100A4 on E-cadherin and further affect the functions of S100A4 in gastric cancer cells.

S100A4 interacts with mutant p53 and affects gastric cancer MKN1 cell autophagy and differentiation.

The acquired p53 mutations are the most common genetic alterations in human cancers. Mutant p53 proteins tend to accumulate, augmenting their oncogenic potential. However, the mechanisms for mutant p53 accumulation are not known.

RPS12-specific shRNA inhibits the proliferation, migration of BGC823 gastric cancer cells with S100A4 as a downstream effector.

Our previous study using suppression subtractive hybridization (SSH), cDNA microarray and semi-quantitative RT-PCR showed that RPS12 was overexpressed in gastric cancer and it was closely related to metastasis. However, the role of RPS12 in gastric cancer is not clear, which led us to conduct the current study to further investigate the effects of RPS12 on the proliferation and migration of gastric cancer cells, and also to explore the underlying molecular mechanisms. RNA interference was used to inhibit the expression of RPS12.

S100A4 protects gastric cancer cells from anoikis through regulation of αv and α5 integrin.

Detachment from the extracellular matrix induces a form of programmed cell death termed anoikis. Resistance to anoikis permits cancer cells to survive in systemic circulation and facilitates their metastasis to distant organs. It is well known that S100A4 is overexpressed in many tumors and involved in tumor metastasis, but the mechanisms of the metastasis-promoting function of S100A4 are not fully understood.

Subcellular distribution of S100A4 and its transcriptional regulation under hypoxic conditions in gastric cancer cell line BGC823.

It is well known that S100A4 is overexpressed in many tumors and involved in tumor invasion and metastasis. But the regulation of it is ill understood. We previously found that hypoxia mimicking cobalt chloride (CoCl(2)) enhanced the mRNA and protein expressions of the S100A4 gene in the gastric cancer cell line BGC823.

Short hairpin RNA-mediated inhibition of S100A4 promotes apoptosis and suppresses proliferation of BGC823 gastric cancer cells in vitro and in vivo.

S100A4 has been found to be over-expressed in gastric cancer and associated with poor prognosis of the patients, yet the exact role and molecular mechanism of S100A4 in gastric cancer has not been determined. We found that S100A4 inhibition by RNAi lead to reduced proliferation and increased apoptosis of gastric cancer cell line BGC823. Intratumoral injection of pS100A4-shRNA suppressed tumor growth in nude mice.

Genetic alterations in the PI3K pathway in prostate cancer.

Alterations in the PIK3CA and PTEN genes were assessed in 40 prostate tumors (radical prostatectomy samples). Genetic analyses in glands of the highest Gleason pattern within each tumor revealed PIK3CA amplification in 13%, PIK3CA mutations in 3%, PTEN homozygous deletion in 13% and PTEN hemizygous deletion in 8% of the cases analyzed. Supporting the view that PTEN and PIK3CA act in the same PI3K signaling pathway, genetic alterations in the PIK3CA and PTEN genes were mutually exclusive, except in one tumor.

[Effect of cobalt chloride on S100A4 expression in human gastric cancer cell BGC823].

S100A4 is an important metastasis-associated gene. Researches have confirmed the close correlation between overexpression of S100A4 gene and gastric cancer's infiltration, lymph node metastasis and in vitro invasiveness of gastric cancer cells. In order to investigate the mechanism of overexpression of S100A4 gene, hypoxia mimetic cobalt chloride (CoCl2) was used to treat gastric cancer cell BGC823, and then the expression of S100A4 mRNA and protein in BGC823 cells were detected by RT-PCR, immunohistochemistry, immunofluorescence, and Western blotting analysis.

Decreased expression of DICER1 in gastric cancer.

Background: The role of epigenetics in gene expression regulation and development significantly enhances our understanding of carcinogenesis. All the tumor related genes may be the target of epigenetical or genetic regulation. We selected some epigenetically regulated genes for cDNA array analysis and observed variability in the expression of the DICER1 gene in distinct stages of gastric cancer.

[Effect of B-RAF-specific RNA interference on gastric cancer BGC823 cell line].

To investigate the influence of B-RAF-specific RNA interference on the proliferation and apoptosis of gastric cancer BGC823 cell line. B-RAF-siRNA and scramble-siRNA were synthesized and transfected into BGC823 cells by TransMessenger. The expression of B-RAF gene and Bcl-2 gene in BGC823 cells was detected by RT-PCR and the level of apoptosis was evaluated in transfected cells by flow cytometry.

Gene expression patterns in gastric cancer.

Objective: To identify gene expression patterns in distinct stages of intestinal-type gastric cancer(GC).

Methods: Gene expression patterns of distinct stages of intestinal-type GC samples from 3 patients were compared with cDNA microarray, which contained 576 genes. There were 506 target genes, which included 51 genes identified from our previous experiment with suppression subtractive hybridization(SSH) and other 455 genes chosen for their important roles in cancers.

Analysis of metastasis suppressing function of E-cadherin in gastric cancer cells by RNAi.

Aim: To study the effect of inhibited E-cadherin expression on invasion of cancer cells.

Methods: We designed the nucleotide sequence of siRNA corresponding to 5' non-coding and coding sequence of E-cadherin. 21-nucleotide dssiRNA was synthesized by in vitro transcription with Ambion Silencer TM siRNA Construction Kit.

[Screening and analysis of associated genes in the carcinogenesis and progression of gastric cancer].

Objective: To screen and analyze the important associated genes in different stages of gastric cancer.

Methods: Using suppression subtractive hybridization (SSH) to screen differentially expressed genes; detecting the expression of genes in different stages of gastric cancer with dot blot hybridization; and verifying the results with semi-quantitative reverse transcriptase-polymerase chain reaction(RT-PCR).

Results: Twenty-six differentially expressed gene fragments were obtained by means of SSH.

[The I1307K mutation and protein expression of APC gene in gastric cancer].

In order to explore the correlation of the abnormalities of tumor suppressor gene APC with the carcinogenesis and progression of gastric cancer. The I1307K mutation of APC gene in gastric cancer was analysed using Amplification Refractory Mutation System PCR(ARMS ,PCR),also the expression of APC protein in gastric cancer of different stages was detected by immunohistochemical method. We found that there wasn't I1307K mutation of APC gene in 62 cases of blood samples of susceptible population in high incidence areas of gastric cancer and 45 cases of gastric cancer tissues.

[Cloning associated genes using microdissection-cDNA PCR-SSH in gastric dysplasia].

Objective: To construct cDNA subtracted libraries from gastric dysplasia and further screen differentially expressed genes.

Methods: Relatively pure dysplasia and normal tissue were procured by manual microdissection, and amplified by cDNA-PCR, which was used to carry on for suppression subtractive hybridization (SSH). Subtracted cDNA fragments were linked with vector, cloned, screened, sequenced, and made homologous search.