We define the weight θ-sheaf R X,θ and reinterpret Morse-Novikov cohomology via sheaf theory. We establish a theorem of Leray-Hirsch type for Morse-Novikov cohomology. Eventually, using them, we prove two blow-up formulas and give the isomorphisms explicitly on (possibly noncompact) complex manifolds.

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In this paper, the concept of balanced manifolds are generalized to reduced complex spaces: the class B and balanced spaces. Compared with the case of Kählerian, the class B is similar to the Fujiki class C and the balanced space is similar to the Kähler space. Some properties about these complex spaces are obtained, and the relations between the balanced spaces and the class B are studied. keywords: class B, balanced space, balanced metric, Fujiki class C AMSC: 32C15, 32C10, 53C55, Proposition 2.2. The class B is invariant under bimeromorphic maps. According to Definition 2.1 and Proposition 2.2, compact balanced manifolds, reduced compact complex spaces in the Fujiki class C and the normalizations of complex spaces in B are all in B. Obviously, if X ∈ B is nonsingular, then X is a balanced manifold.Proposition 2.3. If X and Y are reduced compact complex spaces, then X × Y is in the class B if and only if X and Y are both in the class B.

Mithramycin exhibits certain anticancer effects in glioma, metastatic cerebral carcinoma, malignant lymphoma, chorionic carcinoma and breast cancer. However, its effects on salivary adenoid cystic carcinoma remain unclear. Here, we report that mithramycin significantly inhibited epithelial-to-mesenchymal transition and invasion in human salivary adenoid cystic carcinoma cell lines. The underlying mechanism for this activity was further demonstrated to involve decreasing the expression of the transcription factors specificity protein 1 and SNAI1. Specificity protein 1 is a pro-tumourigenic transcription factor that is overexpressed in SACC-LM and SACC-83 cells, and its expression is inhibited by mithramycin. Moreover, chromatin immunoprecipitation assays showed that specificity protein 1 induced SNAI1 transcription through direct binding to the SNAI1 promoter. In summary, this study uncovered the mechanism through which mithramycin inhibits epithelial-to-mesenchymal transition and invasion in salivary adenoid cystic carcinoma cell lines, namely, via downregulating specificity protein 1 and SNAI1 expression, which suggests mithramycin may be a promising therapeutic option for salivary adenoid cystic carcinoma.