Knockdown of Long Noncoding RNA 01124 Inhibits the Malignant Behaviors of Colon Cancer Cells via miR-654-5p/HAX-1.

Background: Previous studies have shown that long noncoding RNAs (lncRNAs) play a key role in cancer, including colon cancer (CC). However, the exact role of long noncoding RNA 01124 (LINC01124) in CC and its mechanisms of action remain unknown. In this study, we investigated the functional effects and the possible mechanism of LINC01124 in CC. Methods: We first determined the expression of LINC01124 in CC tissues (The Cancer Genome Atlas (TCGA) database) and cell lines (quantitative real-time polymerase chain reaction (qRT-PCR)). Functional analysis via Cell Counting Kit-8 (CCK-8), colony formation, cell cycle, wound healing and Transwell assays were performed, and a mechanistic experiment was performed with the western blotting. The function of LINC01124 was also determined in vivo using nude BALB/c mice. Results: The results showed that LINC01124 was upregulated in CC tissues and cell lines. Functional studies showed that knockdown of LINC01124 significantly suppressed the proliferation, migration, and invasion of colon cancer cells in vitro and in vivo. Subsequent mechanistic experiments indicated that LINC01124 acted as a sponge to suppress microRNA 654-5p, which targeted HAX-1. Downregulation of LINC01124 decreased the expression of HAX-1, and overexpression of the miR-654-5p inhibitor attenuated the sh-LINC01124-induced inhibition of CC cell proliferation, migration, and invasion. Conclusion: Collectively, this study revealed that the knockdown of LINC01124 inhibited the malignant behaviors of CC via the miR-654-5p/HAX-1 axis, suggesting that LINC01124 might be a therapeutic target for CC treatment.

Magnetoencephalography assessment of evoked magnetic fields and cognitive function in subcortical ischemic vascular dementia patients.

OBJECTIVE: To investigate the relationship between cognitive impairment and somatosensory evoked magnetic field and auditory evoked magnetic field changes in elderly male patients with subcortical ischemic vascular dementia (SIVD). METHODS: Magnetoencephalography (MEG) was used to record evoked magnetic field changes from 4 SIVD patients (76-88 years), 3 patients with vascular cognitive impairment with no dementia (VCI-ND; 74-87 years), and 6 healthy volunteers (72-85 years). Latency peaks, equivalent current dipole (ECD) strength, and bilateral ECD position were recorded. The MEG data were superimposed on magnetic resonance imaging to produce magnetic source imaging. RESULTS: Compared to controls, SIVD patients showed increased M20 latency and ECD strength. There were no significant differences in M20 inter-hemispheric positions across diagnostic categories. At M100, SIVD patients showed delayed auditory evoked magnetic field latency compared to controls. However, ECD strength and 3-dimensional inter-hemispheric differences were similar across the groups at the M100 measurement. CONCLUSIONS: Changes in somatosensory and auditory evoked magnetic field changes correlated with cognitive impairment in SIVD patients. Magnetic field latency measures may provide an objective and sensitive index for early dementia detection and monitoring of cognitive function.

[The clinical study of somatosensory evoked magnetic fields in patients with acute cerebral infarction by magnetoencephalography].

OBJECTIVE: To investigate the characteristics of somatosensory evoked magnetic fields (SEF) in patients with acute cerebral infarction by magnetoencephalgraphy (MEG). METHODS: SEFs were recorded from 17 patients with acute cerebral infarction and 18 healthy volunteers using 306-channel whole-head MEG. The electric stimuli were presented with interstimulus intervals of 0.5 s. The peaks of SEF were estimated by equivalent current dipole (ECD), which were superimposed on MRI. RESULTS: M20 was the most elemental components of SEF in all subjects, originating from the area close to the "hand area" of the primary somatosensory cortex. There appeared several abnormal SEF parameters in the patient group: (1) the value of interhemispheric difference of the M20 positions was (8 +/- 4) mm in the normal group and (11 +/- 3) mm in the patient group (P < 0.01); (2) the peak latency of M20 responses in the healthy group was (20.7 +/- 1.1) ms, significantly shorter than those in both the unaffected hemisphere and affected hemisphere in the patient group, (21.8 +/- 1.2) ms and (23.6 +/- 1.9) ms, (both P < 0.01); (3) the strength of ECD in the affected hemisphere was (17 +/- 10) nAm, significantly smaller than that in the unaffected hemisphere, (26 +/- 10) nAm (P < 0.01). CONCLUSION: Latent cortical impairment may be evaluated by MEG with higher spatial and temporal resolution. MEG provides objective and sensitive indexes to evaluate the function of somatosensory cortex in patients with acute cerebral infarction.