Notes

Any Gel-Based Assay regarding Probing Protein Translocation on dsDNA.
Colorectal cancer (CRC) is a common cancer worldwide, and its treatment strategies are limited. The underlying mechanism of CRC progression remains to be determined. Telomere maintenance 2 (TELO2) is a mTOR‑interacting protein. Both the role and molecular mechanism of TELO2 in cancer progression remain unknown. In this study, the gene expression database of normal and tumor tissue, in addition to western blot analysis, and immunohistochemistry (IHC) were used to determine the expression and location of TELO2 in CRC and normal tissues. Clinical features of a tissue array were collected and analyzed. WST‑1, soft agar, flow cytometry, wound healing, and invasion assays were employed to verify the role of TELO2 in the growth, cell cycle, migration, and invasion of CRC cells. The correlation between TELO2 and RICTOR (rapamycin‑insensitive companion of mTOR) was analyzed by bioinformatics, IHC, and immunoprecipitation. Normal and serum‑deprived cells were collected to detect the protein level of TELO2 and its downstream effectors. The results revealed that TELO2 was significantly upregulated in CRC, and TELO2 inhibition significantly restrained the growth, cell cycle, and metastasis of CRC cells. TELO2 overexpression correlated with age, lymph node metastasis, and TNM stage of CRC patients. In addition, TELO2 was positively correlated with RICTOR in CRC and induced tumor progression mainly via RICTOR with serum in culture. RICTOR induced the degradation of TELO2 upon serum deprivation in an mTOR‑independent manner. These findings indicate that TELO2 promotes tumor progression via RICTOR in a serum‑dependent manner, which may be a potential therapeutic target for CRC.Subsequently to the publication of this paper, an interested reader drew to the authors' attention that two pairs of data panels containing strikingly similar data were featured in Fig. 4A and B. The authors have re‑examined their data and realized that Fig. 4 was assembled incorrectly. The revised version of Fig. 4, containing the correct data for Fig. 4A and B, is shown on the next page. The authors regret the errors that were made in the preparation of the published figure, and confirm that these errors did not seriously affect the conclusions reported in the paper. The authors are grateful to the editor of Oncology Reports for allowing them the opportunity to publish a Corrigendum, and all the authors agree to this Corrigendum. Furthermore, they apologise to the readership for any inconvenience caused. [the original article was published in Oncology Reports 39 1356-1368, 2018; DOI 10.3892/or.2017.6169].Keratin 7 (KRT7) is a member of the keratin gene family. KRT7 is abnormally expressed in various types of cancer and promotes the malignant progression of tumors. However, the role of KRT7 in ovarian cancer remains unclear. The present study aimed to validate the role of KRT7 in ovarian cancer progression. KRT7 expression levels in patients with ovarian cancer were analyzed using data obtained from the Human Protein Atlas and The Cancer Genome Atlas databases. KRT7 mRNA and protein expression levels were upregulated in ovarian cancer tissue compared with normal tissue. KRT7 expression was associated with the grading, staging and poor prognosis of ovarian cancer. The differentially expressed genes affected by KRT7 were primarily enriched in the functions of cell migration, cell adhesion and cell growth. In vitro studies, including a CCK8 assay, were used to detect cell proliferation. In addition, wound healing and transwell assays were performed to analyze cell migration. The results demonstrated that KRT7 overexpression was associated with increased proliferation, migration and epithelial‑mesenchymal transition (EMT) of ovarian cancer cells, and the migration and EMT of ovarian cancers cells were decreased following knockdown with KRT7 small interfering RNA. selleck chemicals In vivo, knockdown of KRT7 inhibited tumor growth of ovarian cancer. Furthermore, KRT7 regulated EMT in ovarian cancer via the TGF‑β/Smad2/3 pathway, and regulated cell‑matrix adhesion through integrin‑β1‑focal adhesion kinase signaling. These results suggest that KRT7 may be a potential molecular marker for prognosis prediction in patients with ovarian cancer.The effectiveness of an elemental diet (ED), Elental®, against radiotherapy‑ or chemoradiotherapy‑induced oral mucositis was previously reported. However, the administration of additional nutrition or an ED in patients with oral cancer may also provide extra nutrition for cancer cells, which could result in cancer development. At present, it remains unclear whether the beneficial effects of an ED are likely to surpass its potential harmful effects on oral cancer treatment. In the present study, we aimed to clarify whether Elental® has different effects on a healthy human oral keratinocyte (HOK) cell line compared with its effects on oral squamous cell carcinoma (OSCC) cell lines (HSC2, HSC3, HSC4). The efficacy of Elental® was compared in relation to the growth and migration ability of HOK and OSCC cell lines using MTT assay and migration assay, respectively. In addition, whole transcriptome analysis and network analysis were performed to determine the difference in the mechanism of action of Elental® betweenntal® on healthy oral cells and oral cancer cells may differ.The versatility of IGFBP2, as a secreted protein in cancer cells or a cytoplasmic signaling effector, has been extensively investigated in many malignant cancers. Over the last few decades, IGFBP2, a key member of the IGFBP family, has been identified as an important oncogene in multiple human cancers. In addition, a growing number of studies have shown that IGFBP2 is greatly elevated in serum or tissue in patients with malignant tumors and plays an essential role in several key oncogenic processes, such as tumor cellular proliferation, migration, invasion, angiogenesis, epithelial‑to‑mesenchymal transition, and immunoregulation, which are involved in a variety of signal pathways, usually via an IGF‑independent means. Moreover, growing evidence indicates that aberrant overexpression of IGFBP2 may serve as a useful biomarker for the diagnosis and prognosis of patients, as well as act as a potential therapeutic target for the management of clinical treatment in patients with malignant disease. In the present review, we summarize the current points of view that IGFBP2 performs a role in the initiation and progression of various types of cancer by interacting with several key molecules involved in cancer signaling pathways.
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