Aims:Corona virus disease 2019 has rapidly become the most severe public health issue all over the world. Despite respiratory symptoms, hepatic injury has also been observed in clinical settings. This study aimed to investigate the risk factors involved with hepatic injury in the patients with COVID-19.Methods: A total of 85 hospitalized patients who were diagnosed with COVID-19 in Beijing You'an Hospital were retrospectively analyzed. According to liver function, they were divided into ALT normal group (n=52) and ALT elevation group (n=33).Clinical features and laboratory data were compared between the two groups. The independent risk factors for liver injury were analyzed.Results: There were 33 patients with hepatic injury in our study, accounting for 38.8%(33/85). The patients in ALT elevation group were older than those in ALT normal group. The levels of lactic acid, CRP, myoglobin, and neutrophils were significantly higher in ALT elevation group. The lymphocytes and albumin were significantly lower in ALT elevation group. The proportion of severe and critical patients in ALT elevation group was significantly higher. Multivariate logistic regression analysis showed CRP ≥ 20 mg/L and lymphocyte count< 1.1×10^9/L were independently related to hepatic injury. Conclusions:Lymphopenia and CRP may serve as the risk factors related to hepatic injury in patients with COVID-19, which might be related to inflammatory cytokine storm in liver injury. Early detection and timely treatment of hepatic injury in patients with COVID-19 are necessary.

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TLGsur showed the most powerful predictive performance than the other PET parameters for the prediction of OLM in cN0 lung adenocarcinoma. This normalized volumetric parameter would be helpful in selection of sublobar resection or aggressive tailored treatments in patients with cN0 lung adenocarcinoma.

Chemotherapeutic resistance remains a critical clinical issue is responsible for treatment failure in patients with ovarian cancer. Evidence of the involvement of miRNAs in chemoresistance in ovarian cancer has been recently emerging. However, the underlying molecular links between chemoresistance and miRNAs remain largely unknown. In this study, we report that miR-149-5p expression is markedly elevated in chemoresistant ovarian cancer tissues compared with the chemosensitive ovarian cancer tissues. Furthermore, the silencing of miR-149-5p enhanced the chemosensitivity of ovarian cancer cells to cisplatin in vitro and in vivo. Conversely, the upregulation of miR-149-5p aggravated chemoresistance in ovarian cancer cells. Our results further revealed that miR-149-5p directly targeted the core kinase components of the Hippo signaling pathway, STE20-like kinase (MST)1 and protein salvador homolog 1 (SAV1), resulting in the inactivation of TEA domain (TEAD) transcription. On the whole, our findings reveal a novel mechanism of of action miR-149-5p in inducing chemotherapeutic resistance in ovarian cancer, indicating that miR-149-5p may serve as a chemotherapeutic response indicator and a potential therapeutic target in ovarian cancer.

Circular RNAs (circRNAs) are known to act as key regulators in a variety of malignancies. However, the role of circRNAs in cervical cancer (CCa) remains largely unknown. Herein, we demonstrated that a circRNA derived from the TADA2A gene (hsa_circ_0043280) was significantly downregulated in CCa and that this reduction in expression was correlated with a poor prognosis. Furthermore, our results demonstrated that hsa_circ_0043280 functions as a tumor suppressor to inhibit tumor growth and metastasis in CCa. Mechanistically, hsa_circ_0043280 competitively sponges miR-203a-3p and prevents miR-203a-3p from reducing the levels of PAQR3. Collectively, our results demonstrate that hsa_circ_0043280 plays a pivotal role in the development and metastasis of CCa, thus suggesting that hsa_circ_0043280 has significant potential as a prognostic biomarker and a therapeutic target for CCa.

Src family tyrosine kinase (SFK) activation is associated with ovarian cancer progression. Therefore, SFKs are targets for the development of potential treatments of ovarian cancer. Dasatinib is a tyrosine kinase inhibitor that targets SFK activity, and is used for the treatment of B cell and Abelson lymphomas. At the present time, the potential effect of dasatinib on ovarian cancer is not clear. The aim of the present study was to investigate the antitumor activity of dasatinib, alone and in combination with paclitaxel, in ovarian cancer in vitro and in vivo. In the present study, the expression of Src and phospho-Src-Y416 (p-Src) was measured in six ovarian cancer cell lines using western blotting and immunohistochemistry. In addition, cell viability and apoptosis were measured using an MTT assay and annexin V-fluorescein isothiocyanate staining. An ovarian cancer murine xenograft model was established, in order to evaluate the antitumor effect of dasatinib alone and in combination with paclitaxel in ovarian cancer. High levels of p-Src protein expression were observed in all cell lines, as compared with healthy cells, which indicated activation of the Src signaling pathway. p-Src expression increased in ovarian cancer cells following paclitaxel treatment. Dasatinib treatment demonstrated anti-ovarian cancer properties, by downregulating p-Src expression and by inducing cancer cell apoptosis. Combined treatment with dasatinib and paclitaxel markedly inhibited proliferation and promoted apoptosis of ovarian cancer cells, compared with control cells. Combined dasatinib and paclitaxel treatment exhibited antitumor activities in vivo and in vitro (combination indices, 0.25–0.93 and 0.31–0.75; and tumor growth inhibitory rates, 76.7% and 58.5%, in A2780 and HO8910 cell lines, respectively), compared with paclitaxel treatment alone. Dasatinib monotherapy demonstrated anti-ovarian cancer activities. The effects of dasatinib and paclitaxel treatments on ovarian cancer cells appeared to be mediated by the Src pathway.

Neoadjuvant chemotherapy (NACT) plays an important role in ovarian cancer. The appropriate time interval from the completion of NACT to interval debulking surgery (TTS) in ovarian cancer is still unknown. The aim of this retrospective study was to evaluate the effect of the time interval between the end of NACT and surgery (TTS ≤ 4 weeks vs TTS > 4 weeks) on the survival outcomes among patients with advanced-stage ovarian, tubal, and peritoneal cancers. 152 patients with stage III or IV ovarian, tubal, and peritoneal cancers were included in this retrospective cohort study: 115 in the TTS ≤4 weeks and 37 in the TTS >4 weeks groups. The Kaplan-Meier analysis showed that the progression-free survival in the TTS ≤4 weeks group was longer than that in the TTS >4 weeks group (26 vs 14 months, P=0.04). However, the overall survival was not different between the two groups (66 vs 36 months, P=0.105). The multivariate analysis presented that delay in surgery after NACT (TTS >4 weeks) was associated with a shorter progression-free (P=0.002) but not overall survival (P=0.231). Our findings demonstrated no relationship between the NACT to surgery interval and OS, while a detrimental effect of TTS >4 weeks on PFS was observed.

Bergenin is a secondary metabolite that may be primarily isolated from Bergenia species. Although it has been found to exhibit significant biological activities, the anticancer activity of bergenin against cervical cancer cells has not been explored. The present study was designed to evaluate the anticancer effects of bergenin on HeLa cervical cancer cells. The results showed that bergenin reduced the cell viability of the HeLa cervical cancer cells in a dose-dependent pattern. However, the anticancer effects of bergenin were found to be comparatively lower on the normal cervical cells. Furthermore, the anticancer effects of bergenin were primarily found to be due to induction of apoptosis in the HeLa cervical cancer cells. Notably, bergenin also enhanced the expression of Bax and decreased the expression of Bcl-2. WThe effect of bergenin on cell cycle phase distribution of HeLa cells was also investigated and it was found that bergenin could induce G0/G1 cell cycle arrest. Furthermore, bergenin could also inhibit the migration of HeLa cancer cells as well as the phosphorylation of STAT3. Taken together, bergenin may be a promising candidate for the management of cervical cancer.