In addition, NTS inhibited the expression of nuclear phosphorylated‑STAT3 and its binding to the IL‑6 promoter. Therefore, NTS may be a potential candidate drug for the treatment of inflammation.Spindle assembly abnormal protein 6 homolog (SASS6) is crucial for centriole duplication; however, the role of SASS6 in the proliferation of cancer cells remains unclear. In the present study, the expression and functional role of SASS6 in triple negative breast cancer (TNBC) was assessed. Immunohistochemical staining was performed using an anti‑SASS6 antibody in TNBC and normal tissues. Lentivirus‑mediated RNA interference was used to knockdown SASS6 in MDA‑MB‑231 TNBC cells. Cell viability was determined using an MTT assay, and cell cycle distribution and apoptosis were measured using flow cytometry. Additionally, PathScan intracellular signaling arrays were used to detect the presence of intracellular signaling molecules. The results revealed that SASS6 expression was increased in TNBC tissues compared with the control tissue. Moreover, SASS6 knockdown significantly suppressed the growth of MDA‑MB‑231 cells. MDA‑MB‑231 cell cycle progression was arrested at the G2/M phase and cyclin dependent kinase 1 (CDK1), cyclin B1 and PCNA expression in MDA‑MB‑231 cells was decreased following SASS6 knockdown. Furthermore, the phosphorylation of STAT3, BAD and rpS6 was reduced following SASS6 knockdown. A strong correlation between SASS6 and CDK1 expression was observed in TNBC tissues based on immunohistochemical staining analysis (R=0.989; P less then 0.001). In conclusion, the present study revealed the crucial role of SASS6 in promoting MDA‑MB‑231 cell growth, regulating cell cycle progression and its ability to downregulate the CDK1/cyclin B1 signaling pathway, thus highlighting the potential of SASS6 as a therapeutic target for treatment of TNBC, and merits further investigation in animal models or in preclinical and clinical studies.Tumor‑stroma interactions serve a crucial role in the development of colorectal cancer (CRC), in which secreted protein acidic and rich in cysteine (SPARC) has been implicated.  https://www.selleckchem.com/products/pd0166285.html  Due to interactions between cancer and stromal cells [mesenchymal stem cells (MSCs)], SPARC gene expression is markedly upregulated in CRC cells. The present study investigated the role of SPARC in CRC development and its potential as a biomarker. Specifically, the present study examined the association between SPARC expression and clinicopathological characteristics in 42 cases of CRC. SPARC expression in cancer cells was associated with T grade, N grade (TNM classification), stage and poor prognosis. Furthermore, the area of fibroblast‑activating protein‑positive staining around the cancer cells was increased in SPARC‑positive compared with SPARC‑negative cases. Proliferation and wound healing assays in SPARC‑silenced KM12SM cells [short hairpin RNA SPARC (shSPARC)], the reduced SPARC expression of which was demonstrated by reverse trmation in the tumor microenvironment, suggesting its suitability as a novel target molecule for CRC treatment.Following the publication of the above paper, a concerned reader drew to the Editor's attention that a pair of tumors in Fig. 10 appeared to have been duplicated, although one of the tumors appeared at a larger size in the figure relative to the first one. Furthermore, the flow cytometric plots shown in Fig. 2B in the above paper appeared to be remarkably similar to data presented in a paper published in Phytomedicine [Sui C‑G, Meng F‑D and Jiang Y‑H Antiproliferative activity of rosamultic acid is associated with induction of apoptosis, cell cycle arrest, inhibition of cell migration and caspase activation in human gastric cancer (SGC‑7901) cells. Phyomedicine 22 796‑806, 2015]. After having conducted an independent investigation in the Editorial Office, the Editor of Oncology Reports has determined that the above paper should be retracted from the Journal on account of a lack of confidence concerning the originality and the authenticity of the data. The authors were asked for an explanation to account for these concerns, but the Editorial Office never received any reply. The Editor regrets any inconvenience that has been caused to the readership of the Journal. [the original article was published in Oncology Reports 39 597‑602, 2018; DOI 10.3892/or.2017.6147].Hepatocellular carcinoma (HCC) is a type of primary liver cancer, which is associated with high mortality. HCC is one of the most common malignant tumors worldwide. Cell division cycle 20 (CDC20) has been reported to be associated with the development of various malignant tumors and epithelial‑mesenchymal transition (EMT) has been reported to be involved in the malignant metastasis of HCC. Therefore, the present study hypothesized that CDC20 may participate in the malignant biological behavior of HCC via EMT. The present study analyzed the expression levels of CDC20 in HCC and the association between CDC20 and poor prognosis. Furthermore, the effects of CDC20 on the proliferation, invasion and migration of HCC cells were examined using proliferation, migration and invasion assays. Finally, alterations in EMT were analyzed. The results revealed that CDC20 was highly expressed in HCC and HCC cell lines (P less then 0.05), and its high expression level was significantly associated with poor prognosis in patients with HCC (P less then 0.05). CDC20 silencing inhibited the proliferation, migration and invasion of HCC cells. Furthermore, CDC20 silencing increased the expression levels of E‑cadherin, and decreased the expression levels of N‑cadherin, vimentin and Ki‑67. In conclusion, the present study reported that CDC20 may be a novel therapeutic target in HCC and CDC20 could promote the progression of HCC by regulating EMT.Gingival squamous cell carcinoma (GSCC) is responsible fora large proportion of oral cavity malignancies. GSCC is characterized by rapid cell growth, and progressive invasion and migration. P21 is a widely recognized tumor suppressor, which is induced by P53 activation; however, drugs that aim to promote P21‑mediated tumor suppression remain to be identified. A natural compound library was used to perform broad‑spectrum screening of drugs that could promote P21 expression. Subsequently, the effects of the screened drug on GSCC cell proliferation and apoptosis were evaluated. The results of the present study suggested that lapiferin was the most effective natural compound that promoted the expression of P21 at both mRNA and protein levels. Lapiferin inhibited proliferation and enhanced apoptosis of YD‑38 GSCC cells in a dose‑dependent manner. Furthermore, following treatment with lapiferin, the critical cell cycle regulators cell division cycle 25C and cyclin B1 and tumor cell proliferation markers proliferating cell nuclear antigen and Ki67 were markedly decreased.