miR-183-5p overexpression orchestrates collective invasion in salivary adenoid cystic carcinoma through the FAT1/YAP1 signaling pathway.

The invasion of cancer cells into interstitial tissues in a cohesive unit is termed collective invasion, and it is important for the invasion and metastasis of salivary adenoid cystic carcinoma (SACC). However, the underlying mechanisms regulating SACC collective invasion are still poorly understood. Here, we found that SACC tissues exhibited remarkable FAT1 downregulation and YAP1 upregulation at the invasive front, which was closely associated with collective invasion and distant metastasis.

Artemisinin suppressed tumour growth and induced vascular normalisation in oral squamous cell carcinoma via inhibition of macrophage migration inhibitory factor.

Background: Tumour vascular normalisation therapy advocates a balance between pro-angiogenic factors and anti-angiogenic factors in tumours. Artemisinin (ART), which is derived from traditional Chinese medicine, has been shown to inhibit tumour growth; however, the relationship between ART and tumour vascular normalisation in oral squamous cell carcinoma (OSCC) has not been previously reported.

Methods: Different concentrations(0 mg/kg, 25 mg/kg, 50 mg/kg, 100 mg/kg)of ART were used to treat the xenograft nude mice model of OSCC.

[Corrigendum] Dll4/Notch1 signalling pathway is required in collective invasion of salivary adenoid cystic carcinoma.

Following the publication of this article, the authors have realized that they made an error during the compilation of the images shown in Fig. 6, and that this error was not corrected before the paper was sent to press. Specifically, in Fig.

Insight Into the Molecular Mechanism of Podophyllotoxin Derivatives as Anticancer Drugs.

Podophyllotoxin (PTOX) is a biologically active compound derived from the podophyllum plant, and both it and its derivatives possess excellent antitumor activity. The PTOX derivatives etoposide (VP-16) and teniposide (VM-26) have been approved by the U.S.

CXCL12/CXCR4 facilitates perineural invasion via induction of the Twist/S100A4 axis in salivary adenoid cystic carcinoma.

The activation of CXCL12/CXCR4 axis participated in the progression of multiple cancers, but potential effect in terms of perineural invasion (PNI) in SACC remained ambiguous. In this study, we identified that CXCL12 substantially expressed in nerve cells. CXCR4 strikingly expressed in tumour cells, and CXCR4 expression was closely associated with the level of EMT-associated proteins and Schwann cell hallmarks at nerve invasion frontier in SACC.

CXCR5 induces perineural invasion of salivary adenoid cystic carcinoma by inhibiting microRNA-187.

CXCR5 played critical roles in tumorigenesis and metastasis. Nevertheless, little was known about the involvement of CXCR5 in perineural invasion (PNI) of salivary adenoid cystic carcinoma (SACC). Here, we confirmed upregulation of CXCR5 in SACC specimens and cells and identified that CXCR5 exhibited a significant positive correlation with PNI.

Dll4/Notch1 signalling pathway is required in collective invasion of salivary adenoid cystic carcinoma.

High expression of δ‑like ligand 4 (Dll4) is reportedly related to the invasion, metastasis, and clinical prognosis of various malignant tumours. Our previous study revealed that collective cell invasion was a common pattern in salivary adenoid cystic carcinoma (SACC). However, the roles of the Dll4/Notch1 signalling pathway in the collective invasion of SACC remain unclear.

Plasticity of cancer cell invasion: Patterns and mechanisms.

Cancer cell migration and invasion are integral components of metastatic disease, which is the major cause of death in cancer patients. Cancer cells can disseminate and migrate via several alternative mechanisms including amoeboid cell migration, mesenchymal cell migration, and collective cell migration. These diverse movement strategies display certain specific and distinct hallmarks in cell-cell junctions, actin cytoskeleton, matrix adhesion, and protease activity.

What makes leader cells arise: Intrinsic properties and support from neighboring cells.

Cancer cells collectively invading as a cohesive and polarized group is termed collective invasion, which is a fundamental property of many types of cancers. In this multicellular unit, cancer cells are heterogeneous, consisting of two morphologically and functionally distinct subpopulations, leader cells and follower cells. Leader cells at the invasive front are responsible for exploring the microenvironment, paving the way, and transmitting information to follower cells.

What makes cells move: Requirements and obstacles for leader cells in collective invasion.

Most recently, mounting evidence has shown that cancer cells can invade as a cohesive and multicellular group with coordinated movement, which is called collective invasion. In this cohesive cancer cell group, cancer cells at the front of collective invasion are defined as leader cell that are responsible for many aspects of collective invasion, including sensing the microenvironment, determining the invasion direction, modifying the path of invasion and transmitting information to other cells. To fulfill their dispensable roles, leader cells are required to embark on some specific phenotypes with unusual expression of some proteins and it's very important to investigate into these proteins as they may serve as potential therapeutic targets.

Activation of necroptosis in a rat model of acute respiratory distress syndrome induced by oleic acid.

The present study was aimed to investigate the role of necroptosis in the pathogenesis of acute respiratory distress syndrome (ARDS). The rat model of ARDS was induced by intravenous injection of oleic acid (OA), and observed for 4 h. The lung injury was evaluated by arterial blood gas, lung wet-dry weight ratio (W/D) and histological analyses.

Necrostatin-1 protects against oleic acid-induced acute respiratory distress syndrome in rats.

Necroptosis is a recently discovered necrotic cell death which is regulated by receptor interacting protein kinase 1 (RIPK1) and RIPK3 under the stimulus of death signal and can be inhibited by necrostatin-1 (Nec-1) specifically. Therefore, the aim was to investigate the role of necroptosis in a rat model of acute respiratory distress syndrome (ARDS) induced by oleic acid (OA) and assess the effect of Nec-1 on lung injury in ARDS. Our results found that RIPK1, RIPK3 and mixed lineage kinase domain-like protein (MLKL) were abundantly expressed in rat lung tissues of OA-induced ARDS.

Evaluation of liver function and electroacupuncture efficacy of animals with alcoholic liver injury by the novel imaging methods.

Imaging methods to evaluate hepatic microcirculation (HM) and liver function (LF) by directly monitoring overall liver tissue remain lacking. This study establish imaging methods for LF that combines Laser speckle perfusion imaging (LSPI) and in vivo optical imaging (IVOI) technologies to investigate changes of hepatic microcirculation and reserve function in the animals gavaged with 50% ethanol (15 ml/kg·bw) for a model of acute alcoholic liver injury (ALI), and for evaluation of electroacupuncture (EA) effect. The liver blood perfusion and indocyanine green (ICG) distribution were observe by LSPI and IVOI separately.

[Effect of electroacupuncture of "Taichong" (LR 3) on liver function in mild alcoholic liver injury rats].

Objective: To observe the effect of electroacupuncture (EA) of "Taichong" (LR 3) on liver function in rats with mild alcoholic liver injury (MALI) so as to explore the feasibility of acupuncture in improving mild alcoholic liver injury.

Methods: Forty SD rats were randomly divided into control, model, EA-LR 3 and EA-non-acupoint groups (10 rats/group). MALI model was duplicated by intragastric administration of distillate spirit (14 mL/kg) for 12 hours.