[Retracted] Actin­binding protein anillin promotes the progression of hepatocellular carcinoma in vitro and in mice.

[This retracts the article DOI: 10.3892/etm.2021.9885.].

[Retracted] KIF2C promotes the proliferation of hepatocellular carcinoma cells in vitro and in vivo.

[This retracts the article DOI: 10.3892/etm.2021.10528.].

KIF2C promotes the proliferation of hepatocellular carcinoma cells in vitro and in vivo.

Hepatocellular carcinoma (HCC) is one of the most common malignancies with high mortality and morbidity rates. In recent years, HCC targeted therapy has gained increasing attention. Due to the heterogeneity and high metastasis of HCC, more effective therapeutic targets are needed. Kinesin family member 2C (KIF2C), also known as mitotic centromere-associated kinesin, is a microtubule-based motor protein which is involved in a variety of important cellular processes, such as mitosis. The effects of KIF2C on cancer progression and development have been widely studied; however, its potential effects on HCC remains unclear. In the present study, high expression of KIF2C in human HCC tissues was demonstrated using The Cancer Genome Atlas database and immunohistochemistry assays. KIF2C expression was associated with HCC prognosis, including overall survival and disease-free survival. KIF2C expression was also associated with clinical pathological characteristics including the number of tumor nodes (P=0.015) and tumor size (P=0.009). KIF2C knockdown inhibited the proliferation of HCC cells in vitro, confirmed by MTT and colony formation assays, and suppressed tumor growth in mice which was confirmed by a xenograft mouse model. Together, the results suggested that KIF2C may serve as a promising therapeutic target for the treatment of HCC.

FK506-binding protein 5 promotes the progression of papillary thyroid carcinoma.

OBJECTIVE: To detect the expression of FK506-binding protein 5 (FKBP5) in human papillary thyroid carcinoma (PTC) tissues, and explore its possible role in the progression of PTC. METHODS: FKBP5 expression levels were assessed in 115 PTC tissues and corresponding normal tissues by immunohistochemistry. We also examined the correlations between FKBP5 expression and clinicopathological factors and survival in 75 patients with PTC. The effects of FKBP5 on the proliferation and apoptosis of PTC cells were detected by colony-formation, MTT, and flow cytometry assays, respectively. We further investigated the effects of FKBP5 on tumor growth in mice. RESULTS: We revealed high expression levels of FKBP5 in human PTC tissues compared with normal tissues. Furthermore, high FKBP5 expression was associated with an increased incidence of intraglandular dissemination, and lower overall and progression-free survival. FKBP5 depletion remarkably suppressed the proliferation and induced apoptosis of PTC cells in vitro. FKBP5 further contributed to the growth of PTC tumors in mice. CONCLUSIONS: The results of this study demonstrated the potential involvement of FKBP5 in the progression of PTC, and confirmed FKBP5 as a novel therapeutic target for PTC treatment.

Actin-binding protein anillin promotes the progression of hepatocellular carcinoma in vitro and in mice.

Hepatocellular carcinoma (HCC) is a common type of tumor with high mortality worldwide. Investigations associated with the molecular etiology of HCC and screening novel therapeutic targets are still urgently in need. Anillin (ANLN), as a type of evolutionarily conserved actin-binding protein, is involved in multiple cellular processes. ANLN widely affected the progression and metastasis of several types of cancer, and its overexpression was frequently demonstrated in previous studies. The present study demonstrated high expression of ANLN in human HCC tissues, which was also associated the prognosis of patients with HCC. The associations between ANLN expression and the clinicopathological features were determined, including the number of tumor nodes (P=0.011) and tumor size (P=0.003) of patients with HCC. It was found that ANLN promoted cell proliferation, invasion and migration of HCC cells in vitro, and affected tumor growth in vivo. Therefore, ANLN is suggested as a promising therapeutic target for the treatment of HCC.

Actin-binding protein Anillin promotes the progression of gastric cancer in vitro and in mice.

BACKGROUND: To detect the expression levels of actin-binding protein anillin (ANLN) in human gastric cancer (GC) tissues and explore the possible involvement of ANLN in GC cell proliferation, migration, and invasion. METHODS: The bioinformation analysis was performed in TCGA database to explore the expression of ANLN in human GC tissues and the difference of ANLN expression between multiple types of cancers. IHC assays and clinical pathological analysis were performed to confirm ANLN expression and its correlation with clinical features of GC patients. Colony formation, CCK-8, wound closure, and transwell assays were performed to detect its effects on GC cell proliferation, migration, and invasion in vitro. Tumor growth was also measured using a xenograft animal model. RESULTS: We found the high expression of ANLN in human GC tissues based on the results from TCGA database and IHC staining. We further noticed ANLN depletion resulted in the inhibition of GC cell proliferation, migration, and invasion. Our data further confirmed that ANLN contributed to tumor growth of GC cells in vivo. CONCLUSIONS: We confirmed the involvement of ANLN in GC progression and thought ANLN could serve as a promising therapeutic target for GC.

ASPM predicts poor prognosis and regulates cell proliferation in bladder cancer.

Bladder cancer (BCa) is one of the most common malignancies with high morbidity and mortality worldwide. In recent years, it is of great importance to investigate the molecular etiology associated with of BCa. Abnormal spindle-like microcephaly associated gene (ASPM) is the human orthologous of the Drosophila abnormal spindle (asp) and the most commonly mutated gene of autosomal recessive primary microcephaly. ASPM is overexpressed in several types of cancer cell lines and affects the progression and development of multiple types of cancers. However, its possible role in BCa progression is still unclear. Herein, we demonstrated the possible involvement of ASPM in the progression of BCa. We noticed that high expression of ASPM was positively associated with the poor prognosis. Its knockdown could significantly inhibit the proliferation of BCa cells in vitro and in mice. Therefore, we thought ASPM could act as a promising therapeutic target for BCa.