Long noncoding RNA lncGALM increases risk of liver metastasis in gallbladder cancer through facilitating N‐cadherin and IL‐1β‐dependent liver arrest and tumor extravasation
Huaifeng LiYunping HuYunpeng JinYidi ZhuYajuan HaoFatao LiuYang YangGuoqiang LiXiaoling SongYuanyuan YeShanshan XiangYuan GaoJinhui ZhuYijian ZhangLin JiangWen HuangJian ZhuXiangsong WuYingbin Liu
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Abstract Background Long noncoding RNAs (lncRNA) represent significant factors of the mammalian transcriptome that mediates varied biological and pathological processes. The liver is the most common site for gallbladder cancer (GBC) distant metastasis and contributes to the majority of GBC‐related death. How lncRNA affects GBC metastasis is not completely understood. Results A novel lncRNA termed lncGALM (lncRNA in GBC associated with liver metastasis) was discovered to be highly expressed in cancer patients and xenografted tumors with liver metastasis. Elevated lncGALM in GBC patients also correlated to decreased survival. Invasion and migration of GBC cells were enhanced through lncGALM, both in vitro and in vivo. lncGALM functioned as sponges by competitively binding to and inactivating miR‐200 family members, which increase epithelial‐mesenchymal transition‐associated transcription factor ZEB1 and ZEB2, leading to a fibroblastic phenotype and increased expression of N‐cadherin. In addition, lncGALM bound to IL‐1β mRNA and stabilized the IL‐1β gene that mediates liver sinusoidal endothelial cell (LSECs) apoptosis. lncGALM‐expressing LiM2‐NOZ cells acquired a strong ability to migrate and adhere to LSECs, promoting LSECs apoptosis and therefore facilitating tumor cell extravasation and dissemination. Conclusions lncGALM promotes GBC liver metastasis by facilitating GBC cell migration, invasion, liver arrest, and extravasation via the invasion‐metastasis cascade. Targeting lncGALM may be protective against the development of liver metastasis in GBC patients.Keywords:
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The plasma extravasation inducing activities of several chemical mediators (allergic agents: histamine, leukotriene C4 (LTC4) and platelet activating factor (PAF); neurogenic agents: substance P, capsaicin and carbachol) have been investigated and characterized in rat skin and trachea. Substance P, histamine, LTC4 and PAF induced dose-dependent plasma extravasation in rat skin. The activities of these mediators in inducing tracheal plasma extravasation were very different from those in the skin reactions. When these mediators were injected intravenously, substance P induced severe plasma extravasation, and the activities of histamine and PAF were weaker than that of substance P. When injected intratracheally, only substance P and capsaicin induced tracheal plasma extravasation, while none of the allergic mediators tested caused any plasma extravasation in the trachea. Carbachol did not induce any plasma extravasation in either skin or trachea. These results indicate that the stimulation of afferent substance P-containing nerve fibers has a more important role in the induction of tracheal plasma extravasation than that of allergic chemical mediators.
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Neurogenic inflammation
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Recent studies suggest an active participation of postcapillary venules in inflammatory plasma extravasation. Intravital microscopic studies of rats' incisors show that Evans blue allows the demonstration of plasma extravasation in the dental pulp. This process takes place in the postcapillary venules, as can be seen from the staining of the interstice. Rather than depending on hydrodynamic pressure mechanisms, inflammatory plasma extravasation seems to be subjected to a direct regulation of vascular permeability.
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Objective To describe the risk factors of extravasation, its impact on the pharmacokinetics of non-cytotoxic drugs, and management of extravasation in older individuals. Extravasation occurs when vesicants leak from blood vessels into surrounding tissue causing severe injury such as tissue necrosis while infiltration is caused by leakage of an irritant that causes injury but does not lead to tissue necrosis. Extravasation occurs in approximately 0.01% to 6% of patients, particularly with cytotoxic agents. However, there is limited documentation about extravasation of non-cytotoxic agents, particularly in older people. Data Sources A literature search of Pubmed and Medline was performed using the following search items: "extravasation," "infiltration," "elderly," and "non-cytotoxic drugs," as well as a combination of these terms. Conclusion It is important to recognize, identify, and manage extravasation early since it can have deleterious consequences for older people. It is more important to prevent extravasation than manage it using standardized evidence-based protocols, and this can be implemented in the nursing facility and acute care setting.
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Recent studies suggest an active participation of postcapillary venules in inflammatory plasma extravasation. Intravital microscopic studies of rats' incisors show that Evans blue allows the demonstration of plasma extravasation in the dental pulp. This process takes place in the postcapillary venules, as can be seen from the staining of the interstice. Rather than depending on hydrodynamic pressure mechanisms, inflammatory plasma extravasation seems to be subjected to a direct regulation of vascular permeability.
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Leukocyte extravasation
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Various dye fluids were injected into the blood vessels of frogs and rabbits and observationsin vivo were made of their patterns of extravasation.(1) A relation was noted between the site and mode of extravasation and the diffusibility of dyediffusibility itself being related to the size of dye particles.(2) Following intravenous injection the parts of blood vessels, excepting arterioles, where extravasation can occur were similar with both highly and poorly diffusible dyes. These parts extended from the arterioles to the venules. But the sequence of sites of extravasation and their frequency were in a reverse relationship. With highly diffusible dyes extravasation occurred in the sequence of precapillaries, capillaries, postcapillaries, venules and arterioles, and along the entire course of these vessels, so that the spread of extravasated dyes produced a color band form with the vessels along the long axis of the band. Contrary to this, with poorly diffusible dyes extravasation occurred first from the postcapillaires and venules, especially at the transitional portion of the two, then from the capillaries, and belatedly sometimes from the precapillaries. The mode of extravasation was sporadic and solitary, so that the spread of dye was oval in shape with the vessel running through the axis of the oval.(3) Following intra-arterial injection of highly diffusible dyes leakage of dye occurred in the sequence of arterioles, precapillaries, capillaries and postcapillaries, but not from the venules. With poorly diffusible dyes the sequence was capillaries, pre- and post-capillaries and venules. No leakage occurred from the arterioles. Thus, following intra-arterial injection of any type of dye, extravasation tended to occur in general from the arterial side, when compared with intravenous injection. However, the modes of spread were similar to those following intravenous injection, and highly diffusible dyes escaped from all over the vessels concerned forming a color band, and poorly diffusible dyes sporadically, from here and there, producing oval shaped forms.(4) There was no marked difference in the sites and modes of extravasation between frogs and rabbits.(5) Important factors determing the sites and modes of extravasation were believed to be the size of dye particles and the differences in structure of blood vessel walls according to locality (probably such as the grades in ease of disconnection of the junction between endothelial cells). However, when the local blood flow stops extravasation practically stops, so that the local blood pressure can also be said to promote extravasation. Various physical, chemical, physicochemical and biological factors that influence permeability are also believed to produce changes in size of particles and in structure of blood vessel walls.
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Extravasation
Capsaicin
Neurogenic inflammation
Platelet-activating factor
Leukotriene C4
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