Long non-coding RNA LOC100133669 promotes cell proliferation in oesophageal squamous cell carcinoma.

OBJECTIVES: LOC100133669 is a lncRNA whose function during tumorigenesis remains unclear now. Thus, we aimed to explore its clinical significance and function in oesophageal squamous cell carcinoma (ESCC). MATERIALS AND METHODS: ISH was used to detect LOC100133669 expression in ESCC tissues. The full-length LOC100133669 was identified by using RACE assay. Subcellular distribution of LOC100133669 was examined by nuclear/cytoplasmic RNA fractionation and qPCR. The role of LOC100133669 in ESCC cell growth was determined by colony formation, MTT and flow cytometry experiments in vitro, as well as xenograft tumour experiment in vivo. RNA pull-down assay was performed to find LOC100133669-interacted protein, which was further examined by RIP, IP, Western blot and rescue experiments. RESULTS: LOC100133669 was upregulated in ESCC tissues compared with adjacent non-tumour tissues. High LOC100133669 expression was associated with poor prognosis of patients with ESCC. We defined LOC100133669 to be 831 nt in length and mainly localized in the cytoplasm of ESCC cells. Knockdown of LOC100133669 inhibited ESCC cell proliferation and cell cycle progression, while overexpression of LOC100133669 showed the opposite effects. Furthermore, LOC100133669 could bind to Tim50 and upregulated its protein level through inhibiting ubiquitination. Overexpression of Tim50 in part abolished the LOC100133669 depletion-caused inhibitory effect on ESCC cell proliferation. CONCLUSIONS: LOC100133669 plays an oncogenic role in ESCC and may serve as a promising diagnostic marker and therapeutic target for ESCC patients.

Fructose-bisphosphate aldolase a is a potential metastasis-associated marker of lung squamous cell carcinoma and promotes lung cell tumorigenesis and migration.

Fructose-bisphosphate aldolase A (ALDOA) is a key enzyme in glycolysis and is responsible for catalyzing the reversible conversion of fructose-1,6-bisphosphate to glyceraldehydes-3-phosphate and dihydroxyacetone phosphate. ALDOA contributes to various cellular functions such as muscle maintenance, regulation of cell shape and mobility, striated muscle contraction, actin filament organization and ATP biosynthetic process. Here, we reported that ALDOA is a highly expressed in lung squamous cell carcinoma (LSCC) and its expression level is correlated with LSCC metastasis, grades, differentiation status and poor prognosis. Depletion of ALDOA expression in the lung squamous carcinoma NCI-H520 cells reduces the capabilities of cell motility and tumorigenesis. These data suggest that ALDOA could be a potential marker for LSCC metastasis and a therapeutic target for drug development.

Caveolin-1 interferes cell growth of lung cancer NCI-H446 cell through the interactions with phospho-ERK1/2, estrogen receptor and progestin receptor.

Caveolin-1 (CAV-1) either functions as a tumor suppressor gene or as an oncogene depending on the types of tumor cells and tumors. In current work, we investigated the influences of CAV-1 on the proliferation and cell cycle of small cell lung cancer (SCLC) cell NCI-H446, empty vector transfected NCI-H446 (NCI-H446-neo) and wild-type CAV-1 gene stably transfected NCI-H446 (NCI-H446-CAV-1) cells and explored the potential underlying mechanism. The colony formation capacity of NCI-H446-CAV-1 cell was 58.5% of that for NCI-H446 cell and 57.0% of that for NCI-H446-neo cell. CAV-1 inhibited the cell growth and cell cycle distribution of NCI-H446 cell in vitro. CAV-1 over-expression decreased the population of NCI-H446 cell at S phase and blocked NCI-H446 cell at G2/M phase without apparent effect on G1/G0 cell population. The level of phosphoryalted extracellular signal-regulated kinases (p-ERK1/2) instead of whole ERK1/2 in NCI-H446 cell was dramatically decreased following the stable expression of CAV-1. ERK1/2 phosphorylation might be critical for NCI-H446 cell growth. This work also revealed CAV-1 potentially regulated NCI-H446 growth in a hormone-dependant manner. Estrogen receptor (ER) and progestin receptor (PR) were significantly down-regulated in NCI-H446-CAV-1 cell comparing to NCI-H446 and NCI-H446-neo cells. Taken together, CAV-1 affected cell growth of lung cancer NCI-H446 cell through the interactions with p-ERK1/2, ER and PR.

Higher expression of Caveolin-1 inhibits human small cell lung cancer (SCLC) apoptosis in vitro.

Small cell lung cancer (SCLC) is the most aggressive type of lung cancer, and its treatment is closely associated with apoptosis. Caveolin-1 plays an important role in the development of a variety of human cancers. This study sought to investigate the influence of Caveolin-1 on the apoptosis of SCLC in vitro. We demonstrate that higher expression of Caveolin-1 leads to inhibition of cisplatin and Ultraviolet Radiation (UVR)-induced apoptosis in SCLC cells; and also could decrease caspase-3 activity and increase the stability of Bcl-2 at the protein level. Our findings illuminate a potential molecular mechanism regarding CAV-1's role as anti-apoptosis protein.