Accumulating data indicate caspase-1 (CASP1), one of the inflammatory caspases, promotes hepatocellular carcinoma (HCC) progression in tumor proliferation, invasion, EMT phenotype and sorafenib resistance. However, the molecular basis of regulating caspase-1 expression and caspase-1/IL1B (interleukin-1β) pathway in HCC remains unclear. Here, we demonstrated the novel interplay between caspase-1/IL1B activation and cluster differentiation 44 standard isoform (CD44s) in HCC. In this study, we observed that CD44s is responsible for caspase-1/IL1B activation both in HCC tissues and five HCC cell lines. In normoxia conditions, CD44s knockdown repressed the activation of caspase-1/IL1B via stimulating AMPK-mediated autophagy. Moreover, our data suggested that p62-induced autophagic degradation of caspase-1 accounted for caspase-1/IL1B inactivation in CD44s deficient cells. Administration of recombinant human IL1B could rescue impaired proliferation, invasion, and EMT phenotype in CD44s deficient HCC cells. Lastly, hypoxia-mediated caspase-1/IL1B overexpression could be abolished by CD44s downregulation through decreasing HIF1A and enhancing autophagic activity. Overall, targeting CD44s is a novel inhibitory mechanism of caspase-1/IL1B expression, both in normoxia and hypoxia conditions.

The rock in deep strata of Wuxia area in Junggar Basin is abrasive and with low drillability. Part of the formation sections with abundant fractures, which leads to mud lose frequently. The exploration progress has been slowed down by low drilling speed and accidents. The exploration department of Xinjiang Oilfield Company preferred underbalanced drilling technology on well F8 and A1 on the basis of feasibility analysis of UBD technology in Permian strata. The applications reduced lose circulation effectively and promote the rate of penetration considerably. Well F8 and A1 used foam and nitrogen as underbalanced drilling circulation medium respectively. The wellbore sizes are 215.9 mm. The rate of penetration in underbalanced drilling sections are quintuple than conventional rotary drilling. It saved more than 20 days in the overall drilling time. The conversions between foam/nitrogen with mud were successfully once only. There was no losing circulation during underbalanced drilling progress. The successful application of underbalanced drilling technology in deep strata of Wuxia area solved the deep drilling speed improved problems entirely. It reduced mud lose and promote drilling speed. The drilling overall time and exploration cost has also been decreased greatly. The innovation application provides a new method for deep drilling speed improved in this area. In the passed drilling, the ROP of advanced cone and PDC bits was nearly 0.65 m/h, and the ROP was no more than 0.92 m/h even with turbodrills and impregnated bits. However, the ROP of underbalanced drilling section has promoted several times than conventional drilling. ROP optimizing was substantial versus direct offset wells that experienced quintuple drilling time through the same formation. With this success, the team has accumulated valuable experience of deep drilling for Junggar Basin.

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Growth factor-independent 1 (GFI1) has been reported to serve a vital role in hematopoietic development. However, the function and molecular mechanism of GFI1 in esophageal squamous cell carcinoma (EScc) remains unknown. In the present study, the biological functions and the molecular mechanism of the effects of GFI1 in EScc were analyzed. The results demonstrated that GFI1 expression levels were significantly upregulated in EScc compared with those in normal esophageal tissues. Knockdown of GFI1 using small interfering RNA suppressed EScc cell proliferation and migration. Furthermore, GFI1 enhanced STAT3 and NF-κB signaling by inhibiting the expression of suppressor of cytokine signaling 1 (SOcS1) in EScc cells. Taken together, the results of the present study demonstrated that GFI1 promoted the proliferation and migration of EScc cells via inhibition of SOcS1 expression. These results suggested that GFI1 may be a valuable target for EScc therapy.