MrgprF acts as a tumor suppressor in cutaneous melanoma by restraining PI3K/Akt signaling.

The incidence of cutaneous melanoma (CM) has been increasing annually worldwide. In this study, we identify that MrgprF, a MAS related GPR family member, is decreased in cutaneous melanoma tissues and cell lines due to hypermethylation of its promoter region, and show that patients with CM expressing high levels of MrgprF exhibit an improved clinical outcome. We demonstrate that MrgprF forced expression inhibits tumor cell proliferation, migration, xenograft tumor growth, and metastasis.

Neoadjuvant Immunotherapy for MSI-H/dMMR Locally Advanced Colorectal Cancer: New Strategies and Unveiled Opportunities.

Patients with locally advanced colorectal cancer (LACRC) have a high risk of recurrence and metastasis, although neoadjuvant therapy may provide some benefit. However, patients with high microsatellite instability/deficient mismatch repair (MSI-H/dMMR) LACRC receive little benefit from neoadjuvant chemoradiotherapy (nCRT) or neoadjuvant chemotherapy (nCT). The 2015 KEYNOTE-016 trial identified MSI-H/dMMR as a biomarker indicative of immunotherapy efficacy, and pointed to the potential use of immune checkpoint inhibitors (ICIs).

Insulin-like growth factor 2 mRNA-binding protein 2-stabilized long non-coding RNA Taurine up-regulated gene 1 (TUG1) promotes cisplatin-resistance of colorectal cancer via modulating autophagy.

Long non-coding RNAs (lncRNAs) have been demonstrated to influence the chemoresistance of colorectal cancer (CRC). Therefore, the study is designed to investigate the regulatory function and mechanism of Taurine up-regulated gene 1 (TUG1) in the cisplatin resistance of CRC. qRT-PCR checked the expressions of TUG1, Insulin-like growth factor 2 mRNA-binding protein 2 (IGF2BP2), and miR-195-5p in CRC tissues and cells.

miR-4323 targets hepatoma-derived growth factor (HDGF) to suppress colorectal cancer cell proliferation.

MicroRNAs (miRNAs) are regulators of cancer progression via directly binding to the 3' untranslated region (3'UTR) of target genes to control the activity of signaling network. Recent studies have revealed the function of several miRNAs in colorectal cancer, however, there are still numerous miRNAs which have not been studied yet. Herein, we showed that miR-4323 was a downregulated miRNA according to previous microarray data.

PirB functions as an intrinsic suppressor in hippocampal neural stem cells.

Neural stem cells play pivotal roles during prenatal development and throughout life. Here, we report that Paired immunoglobulin-like receptor B (PirB) functions as a suppressor during brain neurogenesis in the adult mouse. PirB expression increased with age during development, and its deficiency promoted neural stem cell proliferation and differentiation and .

Circ_0026344 restrains metastasis of human colorectal cancer cells via miR-183.

CircRNA circ_0026344 was previously revealed as a tumour-suppressive gene in colorectal cancer (CRC) progression. The purpose of this research was to investigate the role of circ_0026344 in CRC cells metastasis induced by chemokines. Two human CRC cell lines SW480 and Caco-2 were treated by CCL20 and CXCL8.

Erlotinib inhibits colon cancer metastasis through inactivation of TrkB-dependent ERK signaling pathway.

The distal metastasis is the main cause of death in patients with colon cancer. Tyrosine receptor kinase B (TrkB) and ERK signals may be the potential targets for the treatment of colon cancer metastasis. This study aims to investigate whether erlotinib inhibits distant metastasis of colon cancer by regulating TrkB and ERK signaling pathway.

CXCL8 induces epithelial-mesenchymal transition in colon cancer cells via the PI3K/Akt/NF-κB signaling pathway.

The aim of the present study was to investigate the role of chemokine (C-X-C motif) ligand 8 (CXCL8) in the proliferation, invasiveness and metastasis of colon cancer and its role in the induction of epithelial-mesenchymal transition (EMT) via activation of the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/nuclear factor-κB (NF-κB) pathway. The plasmid vector containing CXCL8 cDNA was transfected into LoVo cells using Lipofectamine 2000 reagent. Real-time PCR and western blot analyses were performed to determine expression of CXCL8.

CXCL8, overexpressed in colorectal cancer, enhances the resistance of colorectal cancer cells to anoikis.

Anoikis is a form of apoptosis which occurs when anchorage-dependent cells either show loss of adhesion or inappropriate adhesion. Only a few cancer cells that detach from the primary site of the tumor acquire the ability to resist anoikis and form metastasis. The mechanism underlying the resistance of colorectal cancer (CRC) cells to anoikis remains unclear.

[Influence of preoperative chemoradiotherapy, preoperative chemotherapy, and operation on immunity function in middle or lower rectal cancer patients].

Objective: To study the influence of preoperative chemoradiotherapy, preoperative chemotherapy, and operation alone on the cellular immunity in patients with middle or lower rectal cancer.

Methods: Ninety middle or lower rectal cancer patients were non-randomly divided into 3 equal groups: preoperative radiotherapy group, receiving conventional radiotherapy with a total dose of 30 Gy in 10 fractions completed within 2 weeks; preoperative chemoradiotherapy group, receiving 2 cycles of single-oral drug regimen (capecitabine 1000 mg/m(2) for 2 weeks as a cycle with an interval of 1 week) and then, i.e.