Golgi apparatus (GA) is a very important organelle involved in the metabolism of numerous proteins. TGF-beta1 plays an important role in supporting neuronal survival after ischemic insults. Little is known, however, about the morphological alteration of GA and subcellular compartmentalization of TGF-beta1 in brain after ischemia. Therefore, our present study was designed to check for GA morphological alterations and TGF-beta1 subcellular localization. GA immunoreactivities were examined in the somatosensory cortex of gerbils after 10 min transient forebrain ischemia. Confocal Immunofluorographs of TGF-beta1 and TGN38 were also taken. Results indicated that no fragmentation of GA was found in gerbils of norm, shams and 6, 24 and 72 h postocclusion, but some of the cortical cells showed fragmentation of GA in gerbils 7 days postocclusion. TGF-beta1 was colocalized with TGN38, a marker molecule for the GA. We conclude that there was morphological alterations of GA and TGF-beta1 was present in GA in the somatosensory cortex after 10 min ischemia.
Background
Colorectal cancer (CRC) represents one of the major malignant cancers in the world. It has been demonstrated that long non-coding RNAs (lncRNAs) can cause great influences on various human cancers. Though MCF.2 cell line derived transforming sequence like antisense RNA 1 (MCF2L-AS1) and its carcinogenic effect in CRC has been elucidated by several previous researches, the underlying mechanism remains unknown.
Aim
We aimed at exploring the function and regulatory mechanism of MCF2L-AS1 in CRC.
Methods
MCF2L-AS1 expression in CRC cells was tested via RT-qPCR assay. The effects of MCF2L-AS1 on the biological properties of CRC cells were testified through functional experiments. The molecular mechanism of MCF2L-AS1 was verified through mechanism experiments.
Results
MCF2L-AS1 was highly expressed in CRC cells, and it could enhance the proliferation, migration, invasion and epithelial-mesenchymal transition (EMT) process of CRC cells. MiR-105-5p was sponged by MCF2L-AS1 in CRC cells and Ras-related protein Rab-22A (RAB22A) was verified to be the downstream target of miR-105-5p. It was verified through rescue assays that RAB22A overexpression or miR-105-5p silencing could reverse the repressive impact of MCF2L-AS1 silencing on CRC progression.
Conclusion
MCF2L-AS1 accelerated the malignant development of CRC cells by targeting the miR-105-5p/RAB22A axis.
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