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A previous study implied that long intergenic non-coding RNA 1410 (LINC01410) promotes angiogenesis and metastasis of gastric cancer. However, the role of LINC01410 in colon cancer (CC) has remained elusive. In the present study, LINC01410 was identified to be highly expressed in CC tissues compared to adjacent normal tissues. It was indicated that high expression of LINC01410 in CC tissues was associated with poor prognosis. Further functional study suggested that LINC01410 knockdown significantly reduced the proliferation and invasive capacity of HT-29 and SW620 cells, and inhibited the cell cycle. Regarding the mechanism, LINC01410 was indicated to serve as a sponge for microRNA (miR)-3128, as evidenced by a luciferase reporter assay. Furthermore, knockdown of LINC01410 significantly increased the levels of miR-3128. In addition, miR-3128 was markedly downregulated in CC tissues compared with that in adjacent normal tissues. A rescue assay revealed that inhibition of miR-3128 significantly abrogated the effects of LINC01410 knockdown on CC cell proliferation and invasion. In conclusion, the present study demonstrated that LINC01410 functions as an oncogene in CC, at least in part by directly inhibiting miR-3128.

Abstract. Cancer therapy with rapamycin has been successfully implemented for kidney cancer, glioblastoma and prostate cancer. However, there are few studies concerning the effects of rapamycin on the treatment of human melanoma. In this study, we investigated whether rapamycin may be a promising strategy for the effective treatment of melanoma and explored the possible mechanism for this by culturing M14 cells in vitro and treating with rapamycin at three concentrations (10, 50 or 100 nmol/l). MDC and LC3B staining, western blot analysis, flow cytometry and transmission electron microscopy were employed. We revealed that rapamycin induced autophagy and inhibited the proliferation of M14 cells in a concentration-dependent manner, Furthermore, western blot analysis revealed an upregulated expression of Bcl-2 and downregulated expression of Bax in M14 cells. In conclusion, rapamycin induced autophagy and inhibited the growth of M14 cells. The mechanism may involve regulation of the expression of Bcl-2 family proteins. Rapamycin appears to be a promising strategy for the effective treatment of melanoma.

Gonadotroph adenomas may exhibit qualitative and quantitative defects in gonadotropin biosynthesis and secretion. Hypersecretion of immunoreactive FSH dimers by these adenomas occurs frequently; however, it has not been known whether this FSH is biologically active. Using the granulosa cell aromatase bioassay and a highly specific immunoradiometric assay for FSH, we studied the serum bioactivity and bio- to immunoactivity (B/I) ratios of 14 men with FSH-secreting adenomas and compared these values to those of 11 age-matched normal men. In addition, three adenoma patients received TRH (400 micrograms, iv). The mean basal serum FSH level (international units per L), as measured by both bio- and immunoassays, and the FSH B/I ratios were significantly higher (P less than 0.02, by Kolmogorov-Smirnov test) in the adenoma patients than in normal men (mean +/- SEM; adenoma patients: bioactivity, 68.8 +/- 10.4; immunoreactivity, 34.8 +/- 13.7; B/I ratio, 3.4 +/- 0.6; normal men: bioactivity, 5.8 +/- 1.2; immunoreactivity, 6.4 +/- 0.8; B/I ratio, 0.90 +/- 0.1). Both bio- and immunoactive FSH rose after TRH injection, resulting in maintenance of the B/I (mean +/- SEM; pre-TRH: bio-FSH, 63.7 +/- 22.4; immuno-FSH, 28.0 +/- 14.1; B/I ratio, 2.8 +/- 1.2; post-TRH: bio-FSH, 125.6 +/- 42.7; immuno-FSH, 45.8 +/- 21.8; B/I ratio, 3.5 +/- 1.6). When gonadotroph adenoma cells from three separate patients were cultured and their conditioned media (n = 3) studied, relatively large amounts of both bio- and immuno-FSH were detected. Furthermore, the major isoelectric profile of bio-FSH (pH 4.9-3.0) in the conditioned medium from two such adenomas was shown by chromatofocusing to be comparable to that of purified human pituitary FSH (pH 5.2-3.6). We conclude that gonadotroph adenomas in men secrete FSH that is biologically active, both basally and in response to TRH.

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ABSTRACT. We investigated the effects of stathmin 1 (STMN1) silencing by small interfering (siRNA) on the sensitivity of esophageal cancer cells Eca-109 to paclitaxel. STMN1 siRNA was transiently transfected into Eca-109 cells. The effects of transfection were detected by quantitative polymerase chain reaction and western blotting. The effects of STMN1 silencing by siRNA on the sensitivity of esophageal cancer cells Eca-109 to paclitaxel was tested by MTT and colony formation assays. Hoechst 33258 nuclear staining was used to investigate the differences in Eca-109 cell apoptosis induced by paclitaxel. STMN1 siRNA was successfully transfected and the expression of STMN1 was inhibited. The sensitivity of STMN1 siRNA-transfected Eca-109 cells to paclitaxel was significantly increased (P < 0.01). The apoptosis of Eca-109 cells significantly increased following treatment with paclitaxel (P < 0.01). STMN1 silencing by siRNA may enhance the sensitivity of esophageal cancer cells Eca-109 to paclitaxel and induce apoptosis.

Undifferentiated embryonal sarcoma of the liver (UESL) predominantly occurs in children under the age of 10 years, and ~90% of cases occur in children <15 years old. Patients may complain of abdominal pain, fever or other symptoms. No significant decrease has been identified in the hepatic function or elevation of α-fetoprotein, which differentiates UESL from primary carcinomas of the liver. In the present study, a rare and misdiagnosed case of an UESL arising in a male, which was mistaken for a hepatic abscess and retrospectively re-diagnosed, is reported. This case was misdiagnosed as a hepatic abscess initially, and it was diagnosed as UESL subsequent to performing tests, including a type-B ultrasonic scan and computed tomography (CT), and evaluating pathological findings. The rapid recurrence of the tumor in this patient was identified by CT, and this is associated with the malignancy of the disease. Currently, patients with UESL have a poor prognosis as there is not a successful treatment strategy. The present study analyzes the course of diagnosis and potential treatment for the disease.