Talin1 is an adaptor protein that conjugates integrins to the cytoskeleton and regulates integrins and focal adhesion signaling. Several studies have found that Talin1 is overexpressed in several tumor types and promotes tumor progression. However, the explicit role of Talin1 in hepatocellular carcinoma (HCC) progression is still unclear and its functional mechanism remains largely unknown. In this study, we showed a trend of gradually decreasing expression of Talin1 from normal liver tissues to hepatocirrhosis, liver hyperplasia, the corresponding adjacent non‐tumor, primary HCC, and eventually metastatic foci, indicating that Talin1 may correlate with HCC initiation to progression. Talin1 was significantly downregulated in HCC tissues compared with adjacent non‐tumor tissues and low Talin1 expression was associated with HCC progression and poor prognosis. Furthermore, Talin1 knockdown induced epithelial–mesenchymal transition and promoted migration and invasion in SK‐Hep‐1 cells and HepG2 cells. Mechanistically, we found that the ERK pathway was responsible for these promoting effects of Talin1 knockdown in HCC cells. The promoting effects of Talin1 knockdown on epithelial–mesenchymal transition, migration, and invasion were reversed by U0126, a specific ERK1/2 inhibitor. Taken together, our results suggested that Talin1 might serve as a tumor suppressor in HCC and a potential prognostic biomarker for HCC patients.

No abstract

Objective. To analyze the clinicopathological characteristics associated with radiation-induced cystitis (RIC) in patients with cervical cancer treated with chemoradiotherapy (CRT) alone or postoperational (post-op) CRT. Methods. 107 patients with cervical cancer were retrospectively recruited into the study. The surgical status, FIGO staging, total and fractionated doses of radiotherapy (RT), and multiparameters including the dose, volume irradiated to the total bladder, and bladder wall were evaluated for RIC. The criteria on RIC were referred to CTCAE v5.0. Results. Surgical operation and post-op CRT were delivered in 65 patients and CRT or RT alone in 42 patients. Among those with post-op CRT, 33/34 (97.06%), 22/43 (51.16%), and 10/30 (33.33%) patients were classified as FIGO stage I, II, and III/IV, respectively. The incidence of RIC was 30.84% for the whole group with 87.87% occurred in stage I and II patients. The incidence of CTCAE grade 2 and beyond was significantly higher in patients treated with post-op CRT than those with CRT alone (13.85% vs 2.38%, p  = 0.043). Further analyses showed that the CTCAE level of RIC in the post-op CRT group was related to the relatively smaller average bladder volume ( p  = 0.029), whereas the difference in volume of bladder and bladder wall irradiated to 35.0 Gy or 40.0 Gy was not statistically significant between patients with or without RIC. Conclusion. The combination of surgery and post-op CRT may increase the incidence and severity of radiation-induced cystitis when compared to CRT alone, suggesting that bladder dysfunction associated with surgical procedure might increase the frequency and severity radiation related bladder toxicity. Further study is merited.

No abstract