Knockdown of LINC01087 inhibits gastric cancer malignant behavior by regulating the miR-135a-5p/CAAP1 axis.

Long noncoding RNAs play important roles in the occurrence and development of many malignant cancers. This study focuses on the effects of LINC01087 on gastric cancer and its underlying mechanism. In the present study, LINC01087 and CAAP1 were found to be upregulated, and miR-135a-5p was diminished in gastric cancer specimens and cells. Inhibition of LINC01087 resulted in cell proliferation inhibition and induced cell apoptosis through the intrinsic apoptosis signaling pathway, as evidenced by the activation of caspase-3 and caspase-9. An investigation of the signaling pathway revealed that the effects on proliferation and apoptosis following LINC01087 knockdown were mediated by suppression of CAAP1. Furthermore, application of a miR-135a-5p inhibitor or overexpression of CAAP1 could attenuate the apoptotic effect achieved by LINC01087 inhibition, confirming the involvement of miR-135a-5p/CAAP1 signaling in the occurrence of gastric cancer. In conclusion, the LINC01087/miR-135a-5p/CAAP1 axis modulates gastric cancer tumorigenesis and pathogenesis and presents new insight into gastric cancer targeted therapy.

Influence of different treatment methods of Left Colic Artery on postoperative rehabilitation of patients undergoing Laparoscopic Radical Resection of Rectal Cancer.

Objective: To investigate the effect of different treatment methods of the left colic artery (LCA) on postoperative rehabilitation of patients undergoing laparoscopic radical resection of rectal cancer. Methods: Retrospective analysis was performed on 70 patients undergoing laparoscopic radical resection of rectal cancer who were admitted to The Affiliated Suqian Hospital of Xuzhou Medical University from January, 2020 to December, 2022 were selected and divided into two groups according to different treatment methods of LCA. The preservation group (LCA group) (n=34 cases) and the non-preservation group (NLCA group) (n=36 cases). Both groups were treated with laparoscopic radical resection of rectal cancer. IMA was preserved in the LCA group, but not in the NLCA group. The efficacy indicators, surgical treatment and rehabilitation-related indicators, gastrointestinal hormone indicators (motilin (MTL), gastrin (GAS)), and postoperative complications risk were compared between the two groups before and after surgery. Results: No statistically significant difference was observed between the two groups in terms of efficacy indicators (total number of lymph nodes dissected and number of lymph nodes at the root of the IMA), operation time, intraoperative blood loss, and postoperative drainage tube placement time (p>0.05). However, postoperative anal flatus and hospital stay in the LCA group were considerably shorter than those in the NLCA group (p<0.05). Postoperatively, the levels of MTL and GAS in the two groups were significantly decreased, and the LCA group decreased slightly compared with the NLCA group (p<0.05). Moreover, the incidence of complications in the LCA group (5.88%) was significantly lower than that in the NLCA group (27.78%) (p<0.05). Conclusion: Preservation of LCA and no-preservation of LCA in laparoscopic radical resection of rectal cancer are comparable in terms of therapeutic effect, and the surgery with preservation of LCA is worthy of clinical promotion due to its various benefits such as less impact on gastrointestinal hormone indicators, lower risk of complications, and faster postoperative recovery.

LncRNA TP73-AS1 enhances the malignant properties of colorectal cancer by increasing SPP-1 expression through miRNA-539-5p sponging.

Colorectal cancer (CC) is one of the most aggressive cancers, with a high mortality rate worldwide. This study focuses on the mechanism of CC to explore the effective therapeutic targets. We determined that LncRNA TP73-AS1 (TP-73-AS1) expression was significantly increased in CC tissues. TP73-AS1 silencing dynamically inhibited the proliferation, migratory and invasive capacity in CC cells. Mechanistically, we found that TP73-AS1 targeted miR-539-5p and miR-539-5p silencing could promote the migratory and invasive capacity in CC cells. Further study also confirmed that SPP-1 expression significantly increased after co-transfection of miR-539-5p inhibitors. Knockdown the SPP-1 can reverse malignant properties of CC cells. Si-TP73-AS1 suppressed the tumor growth of CC cells in vivo. In a word, we found that TP73-AS1 enhances the malignant properties of colorectal cancer by increasing SPP-1 expression through miRNA-539-5p sponging. And our study provides a potential therapeutic target of CC.

Relationship between Prognosis with Dynamic Changes of Thyroid Hormone and Cortisol Hormone in Patients with Severe Craniocerebral Injury.

Objective: To analyze the dynamic changes of thyroid hormone and cortisol hormone (COR) and their relationship with prognosis in patients with severe craniocerebral injury. Methods: A retrospective analysis of 48 patients with severe craniocerebral injury who were admitted to our hospital from January 2014 to January 2017 was performed. According to the Glasgow Outcome Scale (GOS) after 3 months of treatment, the patients were divided into a favorable prognosis group (GOS score = 4-5) and a poor prognosis group (GOS score = 1-3). Clinical data such as ICU hospitalization time and mechanical ventilation time between the two groups were collected and compared. The GCS score was evaluated and recorded at 24 h and 7 d after injury, respectively. The fasting venous blood was collected from patients at 24 h and 7 d after injury, and the levels of thyrotropin (TSH), total triiodothyronine (TT3), total thyroxine (TT4), free triiodothyronine (FT3), and free thyroxine (FT4) were detected by the time-resolved fluorescence immunoassay, while the cortisol (COR) levels were examined by the chemiluminescence assays. The prognostic risk factors of patients with severe craniocerebral injury were analyzed using logistic regression analysis. A nomogram prediction model was constructed based on the results of the logistic analysis. The value of each factor in predicting the prognosis of patients with severe craniocerebral injury was analyzed using the ROC curve. Results: Significant differences existed between the poor prognosis group and the favorable prognosis group in age, whether complicated with a cerebral hernia, intracranial hematoma volume, admission time, ICU hospitalization time, GCS score, and mechanical ventilation time (P < 0.05). At 24 h after injury, the levels of TT4, FT3, and FT4 in the poor prognosis group were significantly lower than those in the favorable prognosis group (P < 0.05). On the 7th day after the injury, the levels of FT3, FT4, TT3, TT4, and TSH in the poor prognosis group were prominently lower than those in the favorable prognosis group (P < 0.05). At 24 h after injury, the COR level in the poor prognosis group was observably higher than that in the favorable prognosis group (P < 0.05). Logistic regression analysis showed that age, complicated with a cerebral hernia, length of stay in ICU, FT3, FT4, TT4, and COR were the risk factors affecting the prognosis of patients with severe craniocerebral injury (P < 0.05), while the GCS score was the protective factor (P < 0.05). ROC curve analysis revealed that the area under the curve (AUC) of ICU length of stay, GCS score, FT3, and FT4 to predict the prognosis of patients with severe craniocerebral injury was better with 0.841, 0.885, 0.881, and 0.850, respectively. The survival curve drawn by the K-M method showed that high levels of serum FT3, FT4, and TT4 and low levels of COR were conducive to improve the overall survival time of patients (P < 0.05). Conclusion: Abnormal levels of thyroid hormone and cortisol hormone were found in patients with severe craniocerebral injury. Age, combined brain herniation, ICU length of stay, FT3, FT4, TT4, COR, and GCS scores were all prognostic factors in patients with severe traumatic brain injury. These factors have high value in judging the death and survival of patients with severe craniocerebral injury.

Caspase-3 cleavage of dishevelled induces elimination of postsynaptic structures.

During the development of vertebrate neuromuscular junction (NMJ), agrin stabilizes, whereas acetylcholine (ACh) destabilizes AChR clusters, leading to the refinement of synaptic connections. The intracellular mechanism underlying this counteractive interaction remains elusive. Here, we show that caspase-3, the effector protease involved in apoptosis, mediates elimination of AChR clusters. We found that caspase-3 was activated by cholinergic stimulation of cultured muscle cells without inducing cell apoptosis and that this activation was prevented by agrin. Interestingly, inhibition of caspase-3 attenuated ACh agonist-induced dispersion of AChR clusters. Furthermore, we identified Dishevelled1 (Dvl1), a Wnt signaling protein involved in AChR clustering, as the substrate of caspase-3. Blocking Dvl1 cleavage prevented induced dispersion of AChR clusters. Finally, inhibition or genetic ablation of caspase-3 or expression of a caspase-3-resistant form of Dvl1 caused stabilization of aneural AChR clusters. Thus, caspase-3 plays an important role in the elimination of postsynaptic structures during the development of NMJs.