Cellular communication network 1 promotes CASP2 mRNA expression but suppresses its protein translation in esophageal adenocarcinoma.

Induction of apoptosis in tumor cells is one of the best ways to cure cancer. While most apoptosis requires a chain of caspase activation, CASP2 can do this all by itself. The matricellular protein cellular communication network 1 (CCN1) is known for supporting some cancer growth but suppressing others.

Mouse auditory cortex sub-fields receive neuronal projections from MGB subdivisions independently.

Mouse auditory cortex is composed of six sub-fields: primary auditory field (AI), secondary auditory field (AII), anterior auditory field (AAF), insular auditory field (IAF), ultrasonic field (UF) and dorsoposterior field (DP). Previous studies have examined thalamo-cortical connections in the mice auditory system and learned that AI, AAF, and IAF receive inputs from the ventral division of the medial geniculate body (MGB). However, the functional and thalamo-cortical connections between nonprimary auditory cortex (AII, UF, and DP) is unclear.

The Application of Probe-Based Confocal Laser Endomicroscopy as a Diagnostic Tool in Choledochoscopic Gallbladder-Preserving Surgery.

Background And Aims: Choledochoscopic gallbladder-preserving surgery (CGPS) has the advantage of treating benign gallbladder diseases on the premise of gallbladder preservation. However, it has no reliable preoperative diagnosis if the gallbladder is benign. Probe-based confocal laser endomicroscopy (pCLE) can obtain real-time and clear endoscopic images at the cell level in vivo.

CCN1 suppresses cell proliferation of esophageal squamous cell carcinoma through amyloid precursor protein without DR6 participation.

Esophageal cancer is commonly seen as either squamous cell carcinoma (ESCC) or adenocarcinoma (EAC), two very different cancers. CCN1 is a matricellular protein that induces apoptosis in EAC cells through upregulation of DR5, a death receptor, while its role in ESCC is unclear. DR6 is another death receptor, which has been reported to induce apoptosis, necroptosis, or pyroptosis in various cell systems with or without the engagement of its putative ligand amyloid precursor protein (APP).

TNF upregulates peptidoglycan recognition protein 1 in esophageal cancer cells to clear the path to its signaling: Making the "enemy" a friend.

TNF, CCN1, and peptidoglycan recognition protein 1 (PGLYRP1) are often found together in the inflammatory tissue. While TNF and CCN1 promote tissue regeneration, PGLYRP1 protects it from bacterial infection. In fibroblasts, CCN1 was reported to support TNF in apoptosis induction while PGLYRP1 was found to compete with TNF for binding to TNFR1.

The Role of CCN1 in Esophageal Adenocarcinoma: What We Have Learned From the Lab.

: Esophageal cancer is one of the most common and deadliest cancers in the world, particularly esophageal adenocarcinoma. There has never been a special drug to treat it.: This article summarizes the work that we have done in our laboratory about the role of CCN1 in esophageal cancer and gives a new perspective of CCN1 biology.

From Apoptosis to Necroptosis: The Death Wishes to Cancer.

DNA mutation is a common event in the human body, but in most situations, it is fixed right away by the DNA damage response program. In case the damage is too severe to repair, the programmed cell death system will be activated to get rid of the cell. However, if the damage affects some critical components of this system, the genetic scars are kept and multiply through mitosis, possibly leading to cancer someday.

TNF antagonizes CCN1 in apoptosis in esophageal adenocarcinoma.

TNF signaling mostly supports cell growth by activating NFκB and only induces cell death when NFκB activation fails. CCN1 is a matricellular protein that has been reported capable to convert TNF from a pro-survival factor into a stimulus for cell death without interfering with NFκB signaling. In this study, we examined the relationship between CCN1 and TNF in the context of esophageal adenocarcinoma and found that CCN1 did not help TNF to induce cell death when they were together, instead, it inhibited TNF expression, as well as TNF-induced JNK activation and apoptosis.

Long non-coding RNA LINC00858 inhibits colon cancer cell apoptosis, autophagy, and senescence by activating WNK2 promoter methylation.

Accumulating evidence shows the involvement of long non-coding RNAs (lncRNAs) in tumorigenesis of many types of human cancers. However, the role of LINC00858 in colon cancer has not been fully elucidated. Therefore, we investigated the involvement of LINC00858 in the progression of colon cancer and identified its downstream targets.

Molecular Dynamics in Esophageal Adenocarcinoma: Who's in Control?

Esophageal adenocarcinoma (EAC) is one of the fastest-growing cancers in the world. It occurs primarily due to the chronic gastroesophageal reflux disease (GERD), during which the esophageal epithelium is frequently exposed to the acidic fluid coming up from the stomach. This triggers gene mutations in the esophageal cells, which may lead to EAC development.

Esophageal cancer cells convert the death signal from TRAIL into a stimulus for survival during acid/bile exposure.

Background: TRAIL is best known for killing cancer cells selectively, however, some cancers resist TRAIL treatment for various reasons. Esophageal adenocarcinoma is such an example. Previously, we reported that the tumor cells interrupted TRAIL-mediated apoptosis by overexpressing the decoy receptors and survivin.

Long non-coding RNA HNF1A-AS1 upregulates OTX1 to enhance angiogenesis in colon cancer via the binding of transcription factor PBX3.

Colon cancer shows characteristics of metastasis, which is associated with angiogenesis. Increasing evidence highlights long non-coding RNAs (lncRNAs) as important participants in angiogenesis of cancers, including colon cancer. Hence, this study investigated the role of HNF1A-AS1 in angiogenesis of colon cancer.

Acid/bile exposure triggers TRAIL-mediated apoptosis in esophageal cancer cells by suppressing the decoy receptors and c-FLIP.

Esophageal adenocarcinoma essentially develops from esophageal inflammation caused by chronic GERD. During GERD episodes, the lower esophageal epithelium is repeatedly exposed to stomach acid, which often contains duodenal bile salts that prompt malignant transformation. TRAIL is one of the cytokines produced in response to such insults and targets the transformed cells exclusively.

Overexpression of CCN1 in Het1A cells attenuates bile-induced esophageal metaplasia through suppressing non-canonical NFκB activation.

GERD is the most common gastrointestinal diagnosis given during office visit. People who suffer from a long history of GERD eventually develop Barrett's esophagus, a premalignant intestinal metaplasia due to NFκB activation. Previous studies focused on the contribution of TNF-triggered canonical NFκB pathway to this event.

CCN1 induces apoptosis in esophageal adenocarcinoma through p53-dependent downregulation of survivin.

Many cancer drugs have been developed to control tumor growth by inducing cancer cell apoptosis. However, several intracellular barriers could fail this attempt. One of these barrier is high expression of survivin.

Effectiveness and Safety of the Combination of the Traditional Chinese Medicine Prescription Jade Screen and Desloratadine in the Treatment of Chronic Urticaria: A Systematic Review and Meta-Analysis of Randomized Controlled Trials.

Objective: The aim of this study is to systematically evaluate the clinical efficacy and safety of the traditional Chinese medicine prescription Jade Screen combined with desloratadine in the treatment of chronic urticaria.

Methods: Two researchers independently conducted literature searches. The extracted data were analyzed using Rev Man 5.

CCN1 sensitizes esophageal cancer cells to TRAIL-mediated apoptosis.

TRAIL is one of the best anti-cancer molecules in our body. It kills a variety of cancer cells that are resistant to conventional chemotherapy, without causing much negative impact on normal cells, because its death receptors are almost exclusively found on cancer cells. However, some cancer cells are not sensitive to TRAIL treatment, even though they express its death receptors.

Esophageal malignancy: a growing concern.

Esophageal cancer is mainly found in Asia and east Africa and is one of the deadliest cancers in the world. However, it has not garnered much attention in the Western world due to its low incidence rate. An increasing amount of data indicate that esophageal cancer, particularly esophageal adenocarcinoma, has been rising by 6-fold annually and is now becoming the fastest growing cancer in the United States.

S100A4 in esophageal cancer: is this the one to blame?

Metastasis is the main reason for cancer-related death. S100A4 is one of the key molecules involved in this event. Several studies have shown that overexpression of S100A4 in non-metastatic cancer cells can make them become metastatic, and knockdown of S100A4 in metastatic cancer cells can curtail their invasive nature.

CCN1 Induces β-Catenin Translocation in Esophageal Squamous Cell Carcinoma through Integrin α11.

Aims. Nuclear translocation of β-catenin is common in many cancers including esophageal squamous cell carcinoma (ESCC). As a mediator of Wnt signaling pathway, nuclear β-catenin can activate many growth-related genes including CCN1, which in turn can induce β-catenin translocation.

Serum response factor: look into the gut.

Serum response factor (SRF) is a transcription factor that regulates many genes involved in cellular activities such as proliferation, migration, differentiation, angiogenesis, and apoptosis. Although it has only been known for about two decades, SRF has been studied extensively. To date, over a thousand SRF studies have been published, but it still remains a hot topic.

CCN1 induces a reversible epithelial-mesenchymal transition in gastric epithelial cells.

CCN1 is a matricellular protein that activates many genes related to wound healing and tissue remodeling in fibroblasts, but its effect on epithelial cells remains unclear. This study examined the role of CCN1 in epithelial wound healing using rat gastric epithelial cells and rat stomach ulcer as in vitro and in vivo models, respectively. We found that CCN1 expression is highly upregulated in the epithelial cells adjacent to a wound and remains high until the wound is healed.

CCN1 is critical for acid-induced esophageal epithelial cell transformation.

CCN1 is a matricellular protein involved in both wound healing and cancer cell invasion. Increased CCN1 expression has been associated with the development of Barrett's esophagus and the increased risk of progression to esophageal adenocarcinoma. In both cases, acid reflux is a major contributor.

Potential of casein kinase I in digestive cancer screening.

Casein kinase I is a group of ubiquitous Serine/Threonine kinases that have been implicated in both normal cellular functions and several pathological conditions including Alzheimer's disease and cancer. Recent findings in colon and pancreatic cancer have brought tremendous attention to these molecules as potential therapeutic targets in treatment of digestive cancers. In this review, we summarize up to date what is known about this family of kinases and their involvement in carcinogenesis and other pathological conditions.