Given a passage with a context and an answer, construct a question on the basis of the information present in the passage. Construct the question in such a way that (i) it is unambiguous, (ii) it is answerable from the passage, (iii) its answer is unique (iv) it answer uses text phrases from the passage. Avoid creating questions that (i) can't be answered correctly without actually understanding the passage and (ii) uses the same words or phrases given in the passage.

Q: Context: We utilized whole-genome mapping of promoters that are activated by DNA hypomethylation in hepatocellular carcinoma (HCC) clinical samples to shortlist novel targets for anticancer therapeutics. We provide a proof of principle of this approach by testing six genes short-listed in our screen for their essential role in cancer growth and invasiveness.', 'We used siRNA- or shRNA-mediated depletion to determine whether inhibition of these genes would reduce human tumor xenograft growth in mice as well as cell viability, anchorage-independent growth, invasive capacities, and state of activity of nodal signaling pathways in liver, breast, and bladder cancer cell lines.', 'Depletion of EXOSC4, RNMT, SENP6, WBSCR22, RASAL2, and NENF effectively and specifically inhibits cancer cell growth and cell invasive capacities in different types of cancer, but, remarkably, there is no effect on normal cell growth, suggesting a ubiquitous causal role for these genes in driving cancer growth and metastasis. Depletion of RASAL2 and NENF in vitro reduces their growth as explants in vivo in mice. RASAL2 and NENF depletion interferes with AKT, WNT, and MAPK signaling pathways as well as regulation of epigenetic proteins that were previously demonstrated to drive cancer growth and metastasis.
Answer: Our results prove that genes that are hypomethylated and induced in tumors are candidate targets for anticancer therapeutics in multiple cancer cell types. Because these genes are particularly activated in cancer, they constitute a group of targets for specific pharmacologic inhibitors of cancer and cancer metastasis. Clin Cancer Res; 20(12); 3118-32. ©2014 AACR.

A: Does genome-wide study of hypomethylated and induced genes in patients with liver cancer unravel novel anticancer targets?
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Q: Context: Efficient enzymatic saccharification of plant cell wall material is key to industrial processing of agricultural and forestry waste such as straw and wood chips into fuels and chemicals.', "Saccharification assays were performed on steam-pretreated wheat straw under ambient and O2-deprived environments and in the absence and presence of a lytic polysaccharide monooxygenase (LPMO) and catalase. A kinetic model was used to calculate catalytic rate and first-order inactivation rate constants of the cellulases from reaction progress curves. The addition of a LPMO significantly (P\xa0<\xa00.01, Student's T test) enhanced the rate of glucose release from 2.8 to 6.9\xa0h(-1) under ambient O2 conditions. However, this also significantly (P\xa0<\xa00.01, Student's T test) increased the rate of inactivation of the enzyme mixture, thereby reducing the performance half-life from 65 to 35\xa0h. Decreasing O2 levels or, strikingly, the addition of catalase significantly reduced (P\xa0<\xa00.01, Student's T test) enzyme inactivation and, as a consequence, higher efficiency of the cellulolytic enzyme cocktail was achieved.
Answer: Oxidative inactivation of commercial cellulase mixtures is a significant factor influencing the overall saccharification efficiency and the addition of catalase can be used to protect these mixtures from inactivation.

A: Does catalase improve saccharification of lignocellulose by reducing lytic polysaccharide monooxygenase-associated enzyme inactivation?
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Q: Context: To investigate the potential role of prostasin, as an invasion suppressor, in the process of trophoblast invasion in preeclampsia.', 'This case-control study included 19 early-onset severe preeclampsia (⩽ 34 weeks), 20 late-onset severe preeclampsia (>34 weeks) and 20 normal term pregnant women. Immunohistochemistry was conducted to identify the cellular localization of prostasin, as well as the matrix metalloproteinase 2 (MMP2) and MMP9 in the placenta tissues. Enzyme-linked immunosorbent assay was performed to analyze the expression of these three proteins in placental homogenates. The effect of prostasin on the invasive and migratory ability of trophoblast cells was detected by transwell assays. We also examined the regulation of the prostasin antibody in the MMP2 and MMP9 secretion by HTR-8/SVneo cells via blocking the prostasin activity.', 'This study demonstrated that the prostasin, MMP2 and MMP9 were all expressed in the placental syncytiotrophoblasts. Increased expression of prostasin was detected in cases with early-onset severe preeclampsia compared with the late-onset and control groups (P < 0.05), whereas the expression patterns of MMP2 and MMP9 in placental homogenates were opposite to that of prostasin (P < 0.05). Recombinant prostasin inhibited the invasion and migration of trophoblast cells, whereas prostasin antibody enhanced the MMP2 and MMP9 secretion in a dose- and time-dependent manner.
Answer: These findings suggest that prostasin may suppress the invasion process in preeclampsia by attenuating MMP2 and MMP9 secretion.

A:
Does increased expression of prostasin contribute to early-onset severe preeclampsia through inhibiting trophoblast invasion?
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