Mechanisms of Crustal-Mantle Material and Energy Exchanges: Impacts on Hydrocarbon and Geothermal Resources.

The exchange of matter and energy between crust and mantle significantly influences the formation and development of oil, gas, and geothermal resources. Understanding how these exchanges impact these resources is crucial in geological science. In many oil-rich basins in China, significant accumulations of H, CO, geothermal energy, and other associated resources linked to deep mantle materials or geological processes have been discovered.

MiR-497 promotes metastasis of colorectal cancer cells through Nrdp1 inhibition.

We have recently shown that Nrdp1 inhibits phosphorylation of ErB3 in colorectal cancer (CRC) cells, to suppress epidermal growth factor receptor (EGFR) signaling-stimulated MMP7 activation for CRC metastasis. In this study, we examined the control of Nrdp1 in CRC cells. We detected significant increases in miR-497 in CRC specimen, compared to paired normal colorectal tissue.

Nrdp1 inhibits metastasis of colorectal cancer cells by EGFR signaling-dependent MMP7 modulation.

The molecular mechanism underlying cancer invasiveness and metastasis of colorectal cancer (CRC) remains elusive. Here we reported a strong correlation of the levels of neuregulin receptor degradation protein-1 (Nrdp1) and matrix metalloproteinase-7 (MMP7) in CRC from the patients. We then used a human CRC line, Caco-2, to study the underlying molecular basis.

ERK1/2 activity contributes to gemcitabine resistance in pancreatic cancer cells.

Objective: To test the hypothesis that chemoresistance in pancreatic cancer is mediated via extracellular signal-regulated protein kinase (ERK) 1/2 overactivity.

Methods: The human pancreatic cancer cell lines BxPC3, PANC-1 and a stably gemcitabine-resistant subline, PANC1(GemRes), were treated with combinations of gemcitabine and the ERK1/2 inhibitor, U0126. Phosphorylated (p)ERK1/2 was examined by Western blotting; cell proliferation and apoptosis were quantified.

Mesothelin regulates growth and apoptosis in pancreatic cancer cells through p53-dependent and -independent signal pathway.

Mesothelin, a secreted protein, is overexpressed in some cancers, including pancreatic cancer. Rescent studies have shown that overexpression of mesothelin significantly increased tumor cell proliferation, and downregulation of mesothelin inhibited cell proliferation in pancreatic cancer cells, but its exact function and mechanism remains unclear. The aim of the present study was to evaluate the effects of mesothelin on proliferation and apoptosis in pancreatic cancer cells with different p53 status and to explore its signal pathway.

Knockdown of clusterin sensitizes pancreatic cancer cells to gemcitabine chemotherapy by ERK1/2 inactivation.

Objectives: To study the hypothesis that gemcitabine treatment augments the chemoresistance to gemcitabine by clusterin (sCLU) upregulation. Clusterin inhibition could augment the chemosensitivity of human pancreatic cancer cells by inhibition of clusterin-dependent pERK1/2 activation.

Methods: Clusterin was silenced by serial concentration of OGX-011 transfection in pancreatic cancer MIAPaCa-2 and BxPC-3 cell lines, then treated with serial concentration of gemcitabine.