Objective: This study aims to clarify the mechanical action of cyclin-dependent protein kinase 1 (CDK1) in the development of endometrial carcinoma (EMCA), which may be associated with the phosphorylation of kinesin family member C1 (KIFC1) and further activate the PI3K/AKT pathway. Methods: The protein and gene expression of CDK1 in EMCA tissues and tumor cell lines were evaluated by western blot, quantitative polymerase chain reaction, and immunohistochemistry staining. Next, Cell Counting Kit-8 and colony formation assay detected cell survival and proliferation. Cell migration and invasion were measured by Transwell assay. Cell apoptosis and cell cycle were tested by flow cytometry.Immunofluorescence staining of γH2AX was used to evaluate DNA damage, respectively.Subsequently, a co-immunoprecipitation assay was used to detect the interaction between CDK1 and KIFC1. The phosphorylated protein of KIFC1 and PI3K/AKT was detected by western blot. Finally, the effect of CDK1 on the tumor formation of EMCA was evaluated in a nude mouse xenograft model. Results: CDK1 was highly expressed in EMCA tumor cell lines and tissues, which contributed to cell survival, proliferation, invasion, and migration, inhibited cell apoptosis, and induced DNA damage of EMCA cells dependent on the phosphorylation of KIFC1. Moreover, the CDK1-KIFC1 axis further activated PI3K/AKT pathway. Finally, CDK1 knockdown repressed tumor formation of EMCA in vivo. Conclusion We report that increased CDK1 promotes tumor progression and identified it as a potential prognostic marker and therapeutic target of EMCA.

Objective: This study aims to clarify the mechanical action of cyclin-dependent protein kinase 1 (CDK1) in the development of endometrial carcinoma (EMCA), which may be associated with the phosphorylation of kinesin family member C1 (KIFC1) and further activate the PI3K/AKT pathway. Methods: The protein and gene expression of CDK1 in EMCA tissues and tumor cell lines were evaluated by western blot, quantitative polymerase chain reaction, and immunohistochemistry staining. Next, Cell Counting Kit-8 and colony formation assay detected cell survival and proliferation. Cell migration and invasion were measured by Transwell assay. Cell apoptosis and cell cycle were tested by flow cytometry.Immunofluorescence staining of γH2AX was used to evaluate DNA damage, respectively.Subsequently, a co-immunoprecipitation assay was used to detect the interaction between CDK1 and KIFC1. The phosphorylated protein of KIFC1 and PI3K/AKT was detected by western blot. Finally, the effect of CDK1 on the tumor formation of EMCA was evaluated in a nude mouse xenograft model. Results: CDK1 was highly expressed in EMCA tumor cell lines and tissues, which contributed to cell survival, proliferation, invasion, and migration, inhibited cell apoptosis, and induced DNA damage of EMCA cells dependent on the phosphorylation of KIFC1. Moreover, the CDK1-KIFC1 axis further activated PI3K/AKT pathway. Finally, CDK1 knockdown repressed tumor formation of EMCA in vivo. Conclusion We report that increased CDK1 promotes tumor progression and identified it as a potential prognostic marker and therapeutic target of EMCA.

Objective: This study aims to clarify the mechanical action of cyclin-dependent protein kinase 1 (CDK1) in the development of endometrial carcinoma (EMCA), which may be associated with the phosphorylation of kinesin family member C1 (KIFC1) and further activate the PI3K/AKT pathway. Methods: The protein and gene expression of CDK1 in EMCA tissues and tumor cell lines were evaluated by western blot, quantitative polymerase chain reaction, and immunohistochemistry staining. Next, Cell Counting Kit-8 and colony formation assay detected cell survival and proliferation. Cell migration and invasion were measured by Transwell assay. Cell apoptosis and cell cycle were tested by flow cytometry.Immunofluorescence staining of γH2AX was used to evaluate DNA damage, respectively.Subsequently, a co-immunoprecipitation assay was used to detect the interaction between CDK1 and KIFC1. The phosphorylated protein of KIFC1 and PI3K/AKT was detected by western blot. Finally, the effect of CDK1 on the tumor formation of EMCA was evaluated in a nude mouse xenograft model. Results: CDK1 was highly expressed in EMCA tumor cell lines and tissues, which contributed to cell survival, proliferation, invasion, and migration, inhibited cell apoptosis, and induced DNA damage of EMCA cells dependent on the phosphorylation of KIFC1. Moreover, the CDK1-KIFC1 axis further activated PI3K/AKT pathway. Finally, CDK1 knockdown repressed tumor formation of EMCA in vivo. Conclusion We report that increased CDK1 promotes tumor progression and identified it as a potential prognostic marker and therapeutic target of EMCA.

Objective:To construct the impact factor model of primary traditional Chinese medicine (TCM) health management service quality, and put forward corresponding policy suggestions.Methods:In this cross-sectional study, the typical sampling and random sampling method were used to select 39 insiders of primary TCM health management service from 15 communities in Zhejiang Province from August to October in 2022. Interviews on service projects, implementation effects and impact factors were conducted, the three-level coding of interview record was carried out using the grounded theory research method, a model of impact factor for health management service quality of basic TCM was constructed, and the corresponding policy recommendations were put forward.Results:Based on the open coding of 39 original interview data, a total of 516 reference points were obtained, and 53 initial concepts related to the topic were formed and summarized into 17 first-level categories. Through the summary of main axis coding, 6 main categories of “policy environment”，“health literacy”，“community orientation”，“capacity building”，“health preference” and “conflict of interest” were extracted. The logical correlation between the six main categories were analyzed with selective coding, an impact factor model was constructed in accordance with the story line of factors affecting service quality. The story line of this model was as follows: first, the policy environment was the external guarantee of community TCM service quality; second, as the demand-side of the services, the health literacy and requirement of residents was the regulatory factor for service quality; in addition, the community played the role of the supply-side of the services, the service ability construction was the key factor, and the community functions and target orientation was the internal driving factor, meanwhile, the internal/external conflicts of interest had a negative constraint on the service quality.Conclusions:The guarantee intensity of external policy environment is limited, the service demand side pays insufficient attention, and the service supply side functions are absent at the present stage. It is necessary to improve the external policy environment, deepen the connection between supply and demand sides in the field of TCM health service, promote the capacity building of TCM service at the grass-roots level, balance the interests of relevant departments of TCM service, in order to improve the quality of TCM health management service at the grass-roots level.