Renal cell carcinoma (RCC) is one of the common tumors in the urinary system without effective therapies. Angiomotin (Amot) can interact with Yes-associated protein (YAP) to either stimulate or inhibit YAP activity, playing a potential role in cell proliferation. However, the role of Amot in regulating the proliferation of renal epithelial and RCC cells is unknown. Here, we show that Amot is expressed predominantly in the nucleus of RCC cells and tissues, and in the cytoplasm and nucleus of renal epithelial cells and paracancerous tissues. Furthermore, Amot silencing inhibited proliferation of HK-2 and 786-O cells while Amot upregulation promoted proliferation of ACHN cells. Interestingly, the location of Amot and YAP in RCC clinical samples and cells was similar. Amot interacted with YAP in HK-2 and 786-O cells, particularly in the nucleus. Moreover, Amot silencing mitigated the levels of nuclear YAP in HK-2 and 786-O cells and reduced YAP-related CTGF and Cyr61 expression in 786-O cells. Amot upregulation slightly increased the nuclear YAP and YAP-related gene expression in ACHN cells. Finally, enhanced YAP expression restored proliferation of Amot-silencing 786-O cells. Together, these data indicate that Amot is crucial for the maintenance of nuclear YAP to promote renal epithelial and RCC proliferation.

Ulcerative colitis (UC) is the major type of inflammatory ailment with elevated prevalence worldwide. Dieckol (DEK) is a phlorotannin that is extensively found in marine algae and has been found to have different pharmacological properties. Nevertheless, the impact of DEK in UC has not been investigated earlier. Therefore, we appraised DEK's function in dextran sulfate sodium (DSS)‐induced UC in the mouse. An overall of 30 mice was randomized into 5 equal groups. Control mice treated with a standard diet (group I), colitis mice challenged with 3% of DSS through drinking water for 7 consecutive days (group II), DEK was supplemented via oral gavage from day 1 to 10 at the dosages of 5, 10, and 15 mg/kg b.wt, respectively. All animals were sacrificed on the 11th day. The body weight (bwt), colon length, disease activity index, malondialdehyde (MDA), myeloperoxidase (MPO), and histological features were observed using suitable techniques, and COX‐2 expression was investigated by immunohistochemistry. Moreover, TNF‐α, IL‐1β, p65, IκBα, HO‐1, and Nrf2 expressions were measured using ELISA and RT‐PCR techniques, respectively. DEK treatment to the colitis mice considerably lessened, DSS‐challenged alterations in body weight, DAI, colonic length shortening and histological changes. DEK exhibited potent antioxidant effects due to the reduced MDA and MPO, and Nrf2 expression markers while the HO‐1 marker was augmented. Additionally, DEK also suppressed the expression s of TNF‐α, IL‐1β, and the p‐p65, p‐IκBα, and p65 and augmented the expression of IκBα, which eventually proved the anti‐inflammatory potential of DEK against the DSS‐challenge. Based on these results, DEK has been found effective in mitigating colitis, conceivably alleviating colon inflammation through the NF‐κB inhibition and triggering of Nrf2/HO‐1 signaling cascade.

Splenic metastasis of ovarian cancer appears to be more common in serous cystadenocarcinomas. Splenic metastasis usually occurs postoperatively and simultaneously with dissemination to the greater omentum and pelvic cavity. Compared with other ovarian cancer subtypes, ovarian clear cell adenocarcinoma (OCCA) is rare, accounting for <5% of all ovarian malignancies. OCCA has a distinct histological type with poor prognosis and resistance to platinum-based chemotherapy. In the present study, a case of isolated splenic metastasis of OCCA was reported. A 53-year-old female presented with a mass in the left upper quadrant without any other clinical manifestations. Subsequent abdominal and pelvic computed tomography scans revealed multiple mixed cystic-solid lesions, potentially predicting ovarian malignancy. Pathological tests following ovarian cytoreductive surgery revealed primary OCCA with metastases to the spleen. The current study also reviewed recently published literature on splenic metastasis of ovarian carcinoma and demonstrated that the reported case was a rare case of isolated splenic metastasis of OCCA.

The aim of this study was to explore the clinical characteristics of and treatment strategies for interstitial pneumonia induced by gefitinib in patients with advanced non-small cell lung cancer (NSCLC). The detailed clinical data of one patient with NSCLC and gefitinib-induced interstitial pneumonia were compiled and a review of relevant previous studies was performed. Based on this case report and the review, the clinical characteristics, mechanisms and treatment strategies of this rare disease were analyzed. The analyses showed that older, male patients with a long smoking history, high smoking index and adenocarcinoma (particularly bronchoalveolar carcinoma) were more likely to suffer from interstitial pneumonia while taking gefitinib. The onset time of interstitial pneumonia was 1–2 months subsequent to gefitinib administration. The clinical manifestations included chest tightness, shortness of breath, progressive dyspnea, severe hypoxemia and respiratory failure. Diffuse infiltration and alveolar interstitial shadows were observed on the chest tomography scan. In such circumstances, a timely judgment is required, in addition to the withdrawal of gefitinib treatment and the administration of high-dose glucocorticoids, as well as oxygen inhalation and anti-infective therapies, in order to relieve the symptoms. In conclusion, following the onset of gefitinib-induced interstitial pneumonia, the discontinuation of gefitinib is likely to alleviate the suffering of the majority of patients. Early interstitial pneumonia is not an absolute index for the permanent discontinuation of gefitinib treatment. It is necessary to comprehensively consider the benefits and hazards of gefitinib for the patients.