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This is an open access article under the terms of the Creat ive Commo ns Attri butio n-NonCo mmercial License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited and is not used for commercial purposes. AbstractThere is an urgent need to find novel potential therapeutic targets for the diagnosis and treatment of clear cell renal cell carcinoma (ccRCC) due to its highly invasive ability as a common urological malignant tumor. Circular RNAs (circRNAs) have been indicated as potentially critical mediators in various types of tumor progression. We

Background Kinesins play important roles in the development and progression of many human cancers. The functions and underlying mechanisms of kinesin family member C1 (KIFC1), a member of the kinesin-14 family, in the pathogenesis of hepatocellular carcinoma (HCC) have not been fully elucidated. Methods In this study, 168 HCC samples were first analyzed to examine the association between KIFC1 expression and patient clinicopathological features and prognosis. The role of KIFC1 in HCC cell proliferation and metastasis was investigated both in vivo and in vitro. The upstream regulation and downstream targets of KIFC1 were studied by qRT-PCR, western blotting, coimmunoprecipitation, chromatin immunoprecipitation (ChIP) and dual-luciferase reporter assays. Results KIFC1 was highly expressed in HCC tissues and positively associated with advanced stages and poor prognosis. KIFC1 knockdown suppressed HCC cell proliferation and invasion both in vitro and in vivo. Furthermore, KIFC1 knockdown decreased invadopodia formation and reduced epithelial-mesenchymal transition (EMT). HMGA1, an architectural transcriptional factor, was identified to interact with KIFC1. HMGA1 could bind to the promoters of Stat3, MMP2 and EMT-related genes and promote gene transcription. KIFC1 enhanced HMGA1 transcriptional activity and facilitated HCC proliferation and invasion. Moreover, KIFC1 was activated by TCF-4, and KIFC1 inhibition enhanced HCC cell sensitivity to paclitaxel. Conclusions Our findings suggest that KIFC1, activated by TCF-4, functions as an oncogene and promotes HCC pathogenesis through regulating HMGA1 transcriptional activity and that KIFC1 is a potential therapeutic target to enhance the paclitaxel sensitivity of HCC. Electronic supplementary material The online version of this article (10.1186/s13046-019-1331-8) contains supplementary material, which is available to authorized users.

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Abundant crab burrows in carbon-rich, muddy salt marsh soils act as preferential water flow conduits, potentially enhancing carbon transport across the soil-water interface. With increasing recognition of blue carbon systems (salt marshes, mangroves, and seagrass) as hotspots of soil carbon sequestration, it is important to understand drivers of soil carbon cycling and fluxes. We conducted field observations and flow modeling to assess how crab burrows drive carbon exchange over time scales of minutes to weeks in an intertidal marsh in South Carolina. Results showed that continuous advective porewater exchange between the crab burrows and the surrounding soil matrix occurs because of tidally driven hydraulic gradients. The concentrations of dissolved inorganic (DIC) and organic (DOC) carbon in crab burrow porewater differ with that in the surrounding soil matrix, implying a diffusive C flux in the low-permeability marsh soil. Gas-phase concentrations of CO 2 in $ 300 crab burrows were approximately six times greater than ambient air. The estimated total C export rate via porewater exchange (1.0 AE 0.7 g C m −2 d −1) was much greater than via passive diffusion transport (6.7 AE 2 mg C m −2 d −1) and gas-phase CO 2 release (0.93 mg C m −2 d −1). The burrow-related carbon export was comparable to the regional salt marsh DIC export, groundwater-derived DIC export, and the net primary production previously estimated using ecosystem-scale approaches. These insights reveal how crab burrows modify blue carbon sequestration in salt marshes and contribute to coastal carbon budgets.

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BackgroundUncontrolled proliferation is thought to be the most fundamental characteristic of cancer. Detailed knowledge of cancer cell proliferation mechanisms would not only benefit understanding of cancer progression, but may also provide new clues for developing novel therapeutic strategies.MethodsIn vitro function of MNX1 (Motor neuron and pancreas homeobox 1) in bladder cancer cell was evaluated using MTT assay, colony formation assay, and bromodeoxyuridine incorporation assay. Real-time PCR and western blotting were performed to detect MNX1 and CCNE1/2 expressions. In vivo tumor growth was conducted in BALB/c-nu mice.ResultsWe reported that MNX1 is responsible for sustaining bladder cancer cell proliferation. Abnormal MNX1 upregulation in bladder cancer cell lines and 167 human tissue specimens; high MNX1 expression levels correlated significantly with shorter 5-year overall and relapse-free survival in the bladder cancer patients. Furthermore, MNX1 overexpression accelerated bladder cancer cell proliferation and tumorigenicity both in vitro and in vivo, whereas MNX1 downregulation arrested it. In addition, MNX1 transcriptionally upregulated CCNE1 and CCNE2 by directly bounding to their promoters, which promoted G1–S transition in the bladder cancer cells.ConclusionThese findings reveal an oncogenic role and novel regulatory mechanism of MNX1 in bladder cancer progression and suggest that MNX1 is a potential prognostic biomarker and therapeutic target.Electronic supplementary materialThe online version of this article (10.1186/s13046-018-0829-9) contains supplementary material, which is available to authorized users.