BackgroundTriple-negative breast cancer is a biological subtype of breast cancer, which is unresponsive to conventional chemotherapies and has a poor prognosis. C-Phycocyanin (C-PC), a marine natural purified from Spirulina platensis, has been investigated that has anti-cancer function. The mitogen activated protein kinase (MAPK) pathway plays a crucial role in the development and progression of cancer. Therefore, we would like to study the anti-cancer effects of C-phycocyanin in the treatment of triple-negative breast cancer, and explore the role of MAPK pathway in the anti-tumor effects of C-phycocyanin.MethodsCell proliferation, cell cycle, cell apoptosis and cell migration were explored in breast cancer MDA-MB-231 cell lines. AKT, MAPK and membrane death receptor signaling were evaluated in MDA-MB-231 cell lines.ResultsOur study indicated that C-phycocyanin inhibited cell proliferation and reduced colony formation ability of MDA-MB-231 cells. Furthermore, C-phycocyanin induced cell cycle G0/G1 arrest by decreasing protein expression levels of Cyclin D1 and CDK-2 and increasing protein expression levels of p21 and p27. In addition, C-phycocyanin induced cell apoptotic by activating cell membrane surface death receptor pathway. Besides, C-phycocyanin down-regulated the protein expression levels of cyclooxygenase-2, and further inhibited MDA-MB-231 cells migration. We also found cell death induced by C-phycocyanin was carried through the MAPK signaling pathways. C-Phycocyanin was able to induce MDA-MB-231 cell apoptosis by activating p38 MAPK and JNK signaling pathways while inhibiting ERK pathway.ConclusionsC-Phycocyanin exerted anti-cancer activity via the MAPK signaling pathway in MDA-MB-231 cells.

Guillain-Barré syndrome (GBS) is a neurological disorder characterized by paralysis. Identifying the severity, appropriate therapeutic method, and prognosis of GBS at an early stage is highly important. This study aimed to investigate the modifiable risk factors for the severity of GBS and consequent need for mechanical ventilation (MV) and to identify clinical predictive factors for poor short-term outcomes of severe GBS. 155 GBS patients who were admitted to the Affiliated Yantai Yuhuangding Hospital of Qingdao University during 2014–2020 were enrolled. Demographic, clinical, therapeutic and evolutionary data were collected and were then analyzed using univariate and multivariate regression analyses. Our analytic data demonstrated that the significant clinical predictors of severe GBS were recent history of surgery, older age, cranial nerve impairment, and elevated levels of liver enzymes (p < 0.05). Furthermore, autonomic dysfunction, lower Medical Research Council (MRC) score at nadir, and elevated levels of liver enzymes were significantly associated with MV for severe GBS (p < 0.05), and lower MRC score at nadir and autonomic dysfunction remained significant predictors of MV in severe GBS (p < 0.05). Lastly, recent history of surgery, lower MRC score at admission and at nadir, requirement for MV, and pneumonia during hospitalization were significantly associated with the short-term outcome of severe GBS and that lower MRC score at admission and need for MV were confirmed to be predictors of poor short-term prognosis (p < 0.05). Of note, this study suggested that recent history of surgery is a predictor of severity in GBS patients and is associated with the poor short-term prognosis of severe GBS.

Background: To investigate whether radiomic features from ( 18 F)-fluorodeoxyglucose positron emission tomography/computed tomography [( 18 F)-FDG PET/CT] can predict epidermal growth factor receptor (EGFR) mutation status and prognosis in patients with lung adenocarcinoma.Methods: One hundred and seventy-four consecutive patients with lung adenocarcinoma underwent ( 18 F)-FDG PET/CT and EGFR gene testing were retrospectively analyzed. Radiomic features combined with clinicopathological factors to construct a random forest (RF) model to identify EGFR mutation status. The mutant/wild-type model was trained on a training group (n=139) and validated in an independent validation group (n=35). The second RF classifier predicting the 19/21 mutation site was also built and evaluated in an EGFR mutation subset (training group, n=80; validation group, n=25). Radiomic score and 5 clinicopathological factors were integrated into a multivariate Cox proportional hazard (CPH) model for predicting overall survival (OS). AUC (the area under the receiver characteristic curve) and C-index were calculated to evaluate the model's performance. Results: Of 174 patients, 109 (62.6%) harbored EGFR mutations, 21L858R was the most common mutation type [55.9% (61/109)]. The mutant/wild-type model was identified in the training (AUC, 0.77) and validation (AUC, 0.71) groups. The 19/21 mutation site model had an AUC of 0.82 and 0.73 in the training and validation groups, respectively. The C-index of the CPH model was 0.757. The survival time between targeted therapy and chemotherapy for patients with EGFR mutations was significantly different (P=0.03). Conclusions: Radiomic features based on ( 18 F)-FDG PET/CT combined with clinicopathological factors could reflect genetic differences and predict EGFR mutation type and prognosis.

The novel tumor targeted nano-drug C-PC/CMC-CD59sp nanoparticles were constructed with carbocymethyl chitosan (CMC), C-phycocyanin (C-PC) and CD59 specific ligand peptide (CD59sp). The anti-tumor drug mechanism of the C-PC/CMC-CD59sp NPs was further explored in cervical cancer cells (HeLa and SiHa) in vitro and in vivo. We found that the C-PC/CMC-CD59sp NPs could inhibit the proliferation and induce G0/G1 cell cycle arrest in cervical cancer HeLa and SiHa cells, and the cell proliferation was reduced in a dose-dependent manner. We further found that the C-PC/CMC-CD59sp NPs regulated the cell cycle via up-regulating the expression of p21, and then down-regulating the expressions of Cyclin D1 and CDK4 in vivo. Compared with C-PC and C-PC/CMC NPs, the pro-apoptosis effects of the C-PC/CMC-CD59sp NPs were more significant for HeLa and SiHa cells in vitro. Moreover, the C-PC/CMC-CD59sp NPs up-regulated the expression of cleaved caspase-3 and down-regulated the expression of bcl-2. In addition, compared with C-PC and C-PC/CMC, the C-PC/CMC-CD59sp NPs significantly inhibited MMP-2 protein expression in vivo. Our data suggested that the anti-tumor effects of C-PC/CMC-CD59sp NPs were better than C-PC and C-PC/CMC NPs. Our laboratory constructed a new drug delivery system and proved the effective antitumor effects of C-PC/CMC-CD59sp, which would widen the application of C-PC as a potential anti cervical cancer drug.