Background: Colon cancer is the most frequently lethal cancer in digestive system. Herein, we tested the influences of UNC5B antisense lncRNA 1 (UNC5B-AS1) on colon cancer cell growth and metastasis, along with the regulatory function of UNC5B-AS1 in microRNA-622 (miR-622) expression. Methods: Firstly, UNC5B-AS1 expression in colon cancer tissues and corresponding normal tissues were tested. Then, the influences of silencing UNC5B-AS1 by sh-UNC5B-AS1 transfection on colon cancer HCT116 and Caco-2 cell viability, proliferation, migration, invasion and apoptosis, as well as miR-622 expression were assessed, respectively. Subsequently, whether miR-622 attended to the influences of silencing UNC5B-AS1 on HCT116 and Caco-2 cells were probed. Finally, the activities of AMPK and PI3K/AKT pathways in cells were analysed. Results: UNC5B-AS1 had high expression level in colon cancer tissues. Silencing UNC5B-AS1 repressed HCT116 and Caco-2 cell proliferation, migration and invasion, but boosted cell apoptosis. Moreover, silencing UNC5B-AS1 raised miR-622 expression in HCT116 and Caco-2 cells. miR-622 inhibitor transfection weakened the influences of silencing UNC5B-AS1 on HCT116 and Caco-2 cells. Besides, Silencing UNC5B-AS1 suppressed AMPK and PI3K/AKT pathways via raising miR-622. Conclusion: Silencing UNC5B-AS1 repressed colon cancer growth and metastasis might be through raising miR-622 expression and suppressing AMPK and PI3K/AKT pathways.

This report presents a fully thrombosed giant aneurysm of the posterior inferior cerebellar artery (PICA) mimicking an intracranial tumour in a 9-year-old paediatric patient. Surgical clipping and aneurysmectomy were performed. Postoperative imaging studies confirmed the removal of the lesion and the patient was discharged with no neurological deficits. Our case shows that giant thrombosed aneurysms involving the PICA could be potentially misdiagnosed as neoplasms in children and great care must be exercised when managing such cases.

IntroductionNonprojectile penetrating skull base injuries as a result of falls have rarely been confronted in normal neurosurgery although a few nonmissile injuries have been reported. These kinds of injuries represent a life-threatening emergency.Case presentationWe present an unusual case of a 25-year-old male construction worker who suffered an accidental penetrating skull base injury when he fell on a metal rod while he was walking on a 2-meter-high platform. He was clinically stable at presentation. Skull radiograph showed a solid metallic bar, 30 cm long, that penetrated through the right anguli oris eminence and was lodged low in the right occipital bone.ConclusionPenetrating injury to the head is considered a form of severe traumatic brain injury. Although case of penetrating head injuries as a result of fall from heights are very rare, we anticipate the construction works on high-rise buildings are at maximum risk. We advise that removal of this kind of foreign bodies be done in the theater and not outside because of risk of involvement of larger vessels leading to fatal hemorrhage. We further suggest that patients with nonprojectile injuries should undergo a preoperative computed tomography-angiography to rule out any vascular injury.

Background: Prolyl hydroxylase domain proteins (PHD2) is an oxygen sensor that is able to induce hypoxia-inducible factor-a (HIF-a) degradation under normoxic condition. The present paper designed to reveal the function of PHD2 in hepatocellular carcinoma (HCC) cells proliferation, migration and invasion. Methods: qRT-PCR and Western blot were carried out to see the expression of PHD2 in HCC tissues and cell lines. PHD2 expression in Huh7 and HepG3B cells was overexpressed or suppressed by transfection and then the changes of cell proliferation, migration and invasion were detected by CCK-8 assay, transwell assay and Western blot. Results: PHD2 was highly expressed in HCC tissues and cell lines (Huh7, Hep3B, SK-HEP-1, HCCLM3 and MHCC97) as relative to para-cancerous non-tumour tissues and a normal hepatocyte line MIHA. PHD2 overexpression promoted Huh7 and Hep3B cells viability, migration and invasion. Meanwhile, CyclinD1, c-Myc, MMP-2, MMP-9 and Vimentin were up-regulated, while p53 was down-regulated by PHD2 overexpression. PHD2 silence led to a contrary impact. Further, PHD2 overexpression up-regulated Ras and Raf expression and induced phosphorylation of MEK, ERK, JAK1 and STAT3. Conclusion: PHD2 exhibited pro-tumour functions in HCC cells. PHD2 promoted HCC possibly through Ras/Raf/MEK/ERK and JAK1/STAT3 pathways. HIGHLIGHTS 1. PHD2 is highly expressed in HCC tissue and cell lines; 2. PHD2 promotes the proliferation of Huh7 and HepG3B cells; 3. PHD2 enhances Huh7 and HepG3B cells migration and invasion; 4. PHD2 activates Ras/Raf/MEK/ERK and JAK1/STAT3 signalling.

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