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The town of Shuitou was renowned as the leather capital of China because of its large-scale tanning industry, but the industry’s lack of pollution controls has caused severe damage to the local water system. This study determined 15 priority polycyclic aromatic hydrocarbons (PAHs) in water, sediment, soil, and plant samples collected from Aojiang River and its estuary. The total PAHs ranged from 910 to 1520 ng/L in water samples. The total PAH in sediments were moderate to low in comparison with other rivers and estuaries in China, but the relative proportions of PAHs per million people are high when considering the population size associated with each watershed. Ratios of fluoranthene/pyrene and PAHs with low/high molecular weight suggest a petrogenic PAH origin. The PAH composition profile in soil was similar to that in sediment with 4–6 ring PAHs being dominant. The PAHs with 2–3 rings were the dominant species in plant leaves. There were no correlations between PAHs in soils and in plants, suggesting that PAHs accumulate in plant leaves through absorption from the air. The general observation of elevated PAH concentrations in all matrix suggests a possible contribution by the local leather industry on the PAH concentrations in the Aojiang watershed.

Metadherin (MTDH) is a multifunctional oncogene involved in tumor cell migration and metastasis through regulating a number of oncogenic signaling pathways in various human malignancies. Previous studies have demonstrated that MTDH is overexpressed in human colorectal cancer (CRC) and associated with cancer progression and a poor prognosis. However, the underlying mechanisms remain largely unknown. The present study investigated the expression and role of MTDH in CRC cells as well as the underlying mechanism of this. Western blot analysis and quantitative polymerase chain reaction were conducted to determine protein and mRNA expression of MTDH in three human CRC cell lines. A short hairpin RNA (shRNA) targeting MTDH was introduced into CRC HCT116 cells to stably inhibit MTDH expression. A Cell Counting Kit‑8 assay, colony formation assay, Transwell assay and flow cytometry were used to investigate the effect of MTDH‑knockdown on cell proliferation, migration, apoptosis and cell cycle arrest. Western blotting was performed to examine the protein expression levels of cell growth‑ and apoptosis‑associated genes. The results demonstrated that MTDH was commonly expressed in CRC cell lines. MTDH silencing significantly suppressed cell growth, colony forming ability and migration while inducing the apoptosis of HCT116 cells. In addition, MTDH depletion induced S phase cell cycle arrest in HCT116 cells. Mechanistically, knockdown of MTDH markedly downregulated the expression of phosphorylated protein kinase B, c‑Myc, proliferating cell nuclear antigen and B‑cell lymphoma 2 (Bcl‑2) protein in HCT116 cells, and the expression of p53 and Bcl‑2‑associated X protein was significantly increased compared with the negative control shRNA group (P<0.05), suggesting that MTDH may function through the expression of numerous types of apoptosis‑associated and signaling channel proteins in CRC cells. Taken together, these data indicated that MTDH may serve as a biomarker and candidate therapeutic target for CRC.

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