Oral tongue squamous cell carcinoma (OTSCC) is still associated with a poor prognosis due to local recurrence and metastasis. Cancer-associated fibroblasts (CAFs) play an important role in the complex processes of cancer stroma interaction and tumorigenesis. This study aims to determine the role of CAFs in the development and progression of OTSCC. Immunohistochemistry was performed to evaluate the frequency and distribution of CAFs in 178 paraffin specimens from patients with OTSCC. Immunofluorescence, a cell proliferation assay, flow cytometry, migration and invasion assays and western blot analysis were used to study the effects of CAFs and the corresponding conditioned medium (CM) on the proliferation and invasion of OTSCC cell lines. Statistical analysis showed a strong correlation between the frequency and distribution of CAFs and the clinicopathological characteristics of patients with cN0 OTSCC, including pathological stage (P = 0.001), T classification (P = 0.001), and N classification (P = 0.009). Survival analysis demonstrated a negative correlation of the frequency and distribution of CAFs with the overall survival and disease-free survival of patients with cN0 tongue squamous cell cancer (P = 0.009, 0.002, respectively); Cox regression analysis showed that the presence of CAFs (relative risk: 2.113, CI 1.461–3.015, P = 0.023) is an independent prognostic factor. A functional study demonstrated that CAFs and CM from CAFs could promote the growth, proliferation, mobility, invasion and even Epithelial Mesenchymal Transition (EMT) of OTSCC cells compared with NFs and CM from NFs. CAFs were an independent prognostic factor for patients with OTSCC. Compared with NFs, CAFs and their CM have the ability to promote the growth, proliferation, metastasis and even EMT of OTSCC cells.

Background: Overexpression of GOLPH3 (Golgi phosphoprotein 3, 34 kDa) is associated with the progression of many solid tumor types leading to an unfavorable clinical outcome. We aimed to investigate the clinical significance of GOLPH3 expression in the development and progression of clinically N0 (cN0) oral tongue cancer. Methods: Real-time PCR and Western blotting analyses were employed to examine GOLPH3 expression in four oral tongue cancer cell lines, primary cultured normal tongue epithelial cells (TEC), eight matched pairs of oral tongue cancer samples and adjacent noncancerous tissue samples from the same patient. Immunohistochemistry (IHC) was performed to examine GOLPH3 protein expression in paraffin-embedded tissues from 179 cN0 oral tongue cancer patients. Statistical analyses were applied to evaluate the diagnostic value and the associations of GOLPH3 expression with clinical parameters. Results: GOLPH3 mRNA and protein was up-regulated in oral tongue cancer cell lines and cancerous tissues compared with that in primary cultured normal tongue epithelial cells (TEC) and adjacent noncancerous tissue samples. GOLPH3 protein level was positively correlated with clinical stage (P = 0.001), T classification (P = 0.001), N classification (P = 0.043) and recurrence (P = 0.009). Patients with higher GOLPH3 expression had shorter overall survival time, whereas those with lower GOLPH3 expression had longer survival time. Conclusion: Our results suggest GOLPH3 overexpression is associated with poor prognosis for cN0 oral tongue cancer patients and may represent a novel and useful prognostic indicator for cN0 oral tongue cancer.

Background: Ovarian cancer is a frequently-occurring reproductive system malignancy in females, which leads to an annual of over 100 thousand deaths worldwide. Methods: The electronic databases, including GEPIA, ONCOMINE, Metascape, and Kaplan-Meier Plotter, were used to examine both survival and transcriptional data regarding the cell division cycle associated (CDCA) gene family among ovarian cancer patients. Results: All CDCA genes expression levels were up-regulated in ovarian cancer tissues relative to those in non-carcinoma ovarian counterparts. Besides, CDCA5/7 expression levels were related to the late tumor stage. In addition, the Kaplan-Meier Plotter database was employed to carry out survival analysis, which suggested that ovarian cancer patients with increased CDCA2/3/5/7 expression levels had poor overall survival (OS) (P<0.05). Moreover, ovarian cancer patients that had up-regulated mRNA expression levels of CDCA2/5/8 had markedly reduced progression-free survival (PFS) (P<0.05); and up-regulated CDCA4 expression showed remarkable association with reduced post-progression survival (PPS) (P<0.05). Additionally, the following processes were affected by CDCA genes alterations, including R-HAS-2500257: resolution of sister chromatid cohesion; GO:0051301: cell division; CORUM: 1118: Chromosomal passenger complex (CPC, including CDCA8, INCENP, AURKB and BIRC5); CORUM: 127: NDC80 kinetochore complex; M129: PID PLK1 pathway; and GO: 0007080: mitotic metaphase plate congression, all of which were subjected to marked regulation since the alterations affected CDCA genes. Conclusions: Up-regulated CDCA gene expression in ovarian cancer tissues probably played a crucial part in the occurrence of ovarian cancer. The up-regulated CDCA2/3/5/7 expression levels were used as the potential prognostic markers to improve the poor ovarian cancer survival and prognostic accuracy. Moreover, CDCA genes probably exerted their functions in tumorigenesis through the PLK1 pathway.

Oral cancer is a common type of head and neck cancers. Knowing its epidemiologic characteristics is crucial to preventing, diagnosing, and treating this cancer. This study aimed to explore the epidemiologic characteristics of oral cancer in South China. We retrospectively analyzed data from 4097 oral cancer patients treated at the Sun Yat-sen University Cancer Center between 1960 and 2013. We compared the age of onset, sex ratio, pathologic type, and primary tumor location among three subcultural areas (Guangfu, Hakka, and Chaoshan) and between an economically developed region and a less-developed one in Guangdong. Overall, oral cancer had a male-to-female ratio of approximately 2:1, and this ratio decreased over time. Oral cancer occurred mostly in patients of 45–64 years old (54.5%), and the percentage of older patients gradually increased over time. The most common tumor location was the tongue. Squamous cell carcinoma was the predominant pathologic type. The percentage of blood type O in oral cancer patients was lower than that in the healthy population. The male-to-female ratio in the Chaoshan area was higher than that in the Guangfu and Hakka areas, whereas the age of disease onset in Guangfu was higher than that in Hakka and Chaoshan. The male-to-female ratio was lower and the age of disease onset was higher in the economically developed region than in the less-developed region. The incidence of oral cancer in South China presents typical characteristics to which doctors should pay attention when diagnosing and treating oral cancer patients.

S100 calcium‑binding protein A9 (S100A9), a member of the S100 protein family, is often upregulated in various cancers, including cervical cancer. Elevated S100A9 expression is thought to serve an important role in tumorigenesis; however, the exact role of S100A9 in the modulation of cervical cancer and the underlying molecular mechanism remain unknown. In the present study, we aimed to investigate the effects of S100A9 on the proliferation and migration of cervical cancer cells, as well as the molecular mechanisms underlying these effects. Our results demonstrated that endogenous expression of S100A9 in SiHa and CaSki cell lines was significantly higher than in the HeLa cell line. As expected, overexpression of S100A9 enhanced the proliferation and migration of cervical cancer cells. In addition, S100A9 overexpression induced epithelial‑mesenchymal transition (EMT) as determined by reduced expression levels of the epithelial marker E‑cadherin, whereas the expression levels of the mesenchymal marker vimentin were upregulated. Furthermore, it was reported that the effects of S100A9 in the modulation of cervical cancer cells were mediated through the Wnt/β‑catenin signaling pathway as β‑catenin knockdown significantly suppressed the ability of S100A9 to enhance the proliferation and migration of cervical cancer cells. Collectively, these findings suggest that S100A9 promoted the proliferation and migration of cervical cancer cell lines. Furthermore, the underlying molecular mechanisms may be partially attributed to the induction of EMT and activation of the Wnt/β‑catenin signaling pathway.

Background. Lung cancer (LC) has become the top cause responsible for cancer‐related deaths. Cell division cycle-associated (CDCA) genes exert an important role in the life process. Dysregulation in the process of cell division may lead to malignancy. Methods. Transcriptional data on CDCA gene family and patient survival data were examined for lung cancer (LC) patients from the GEPIA, Oncomine, cBioPortal, and Kaplan–Meier Plotter databases. Results. CDCA1/2/3/4/5/7/8 expression levels were higher in lung adenocarcinoma tissues, and the CDCA1/2/3/4/5/6/7/8 expression levels were increased in squamous cell LC tissues compared with those in noncarcinoma lung tissues. The expression levels of CDCA1/2/3/4/5/8 showed correlation with tumor classification. The Kaplan–Meier Plotter database was employed to carry out survival analysis, indicating that increased CDCA1/2/3/4/5/6/7/8 expression levels were obviously related to poor overall survival (OS) and progression‐free survival (PFS) (P < 0.05). Only LC patients with increased CDCA3/4/5/8 expression were significantly related to lower post‐progression survival (PPS) (P < 0.05). The following processes were affected by CDCA genes’ alteration: R‐HAS‐2500257: resolution of sister chromatid cohesion; GO:0051301: cell division; CORUM: 1118: chromosomal passenger complex (CPC, including CDCA8, INCENP, AURKB, and BIRC5); CORUM: 127: NDC80 kinetochore complex; M129: the PID PLK1 pathway; and GO: 0007080: mitotic metaphase plate congression, all of which were remarkably modulated since the alterations affected CDCA genes. Conclusions. Upregulated CDCA genes’ expression levels in LC tissues probably play a crucial part in LC oncogenesis. The upregulated CDCA genes’ expression levels are used as the potential prognostic markers to improve patient survival and the LC prognostic accuracy. CDCA genes probably exert their functions in tumorigenesis through the PLK1 pathway.