AT-rich interaction domain 5A regulates the transcription of interleukin-6 gene in prostate cancer cells.

BACKGROUND: Interleukin-6 (IL-6) is a pleiotropic cytokine that confers androgen-independence and aggressiveness in prostate cancer (PCa); however, the molecular mechanisms regulating IL-6 expression remain unclear. The expression of ARID5A, an AT-rich interaction domain (ARID) DNA-binding motif-containing transcription factor is positively correlated with IL-6 expression in human PCa. We, therefore, hypothesized that ARID5A could regulate IL-6 expression in PCa. METHODS: The relationship between ARID5A and IL-6 in PCa patients was analyzed using statistical analyses of multiple clinical microarray data sets. To investigate whether ARID5A regulates IL-6 expression, CRISPR-driven ARID5A knockout clones were established in DU145 and PC-3 cells. RESULTS: Analysis of three microarray data sets showed a positive correlation between ARID5A and IL-6 expression. The expression of IL-6 in ARID5A knockout clones was significantly reduced compared with control clones in both PCa cell lines. Knockout of ARID5A did not result in any loss of IL-6 mRNA stability. Instead, we observed a significant decrease in the occupancy of both active RNA Polymerase II and the active histone mark, H3K4me3 at the IL-6 transcriptional start site in ARID5A knockout PCa cells, suggesting a role for transcriptional regulation. CONCLUSIONS: Our study demonstrated that loss of ARID5A downregulates the expression of IL-6 at the transcriptional level.

Down-regulation of PADI2 prevents proliferation and epithelial-mesenchymal transition in ovarian cancer through inhibiting JAK2/STAT3 pathway in vitro and in vivo, alone or in combination with Olaparib.

BACKGROUND: Epithelial ovarian cancer (EOC) is the most lethal disease among female genital malignant tumors. Peptidylarginine deiminase type II(PADI II) has been shown to enhance a variety of cancers carcinogenesis, including ovarian cancer. The purpose of this study was to investigate the biological role of PADI2 in ovarian cancer (OC) and the relative mechanism. METHODS: Gene Expression Profiling Interactive Analysis (GEPIA) ( https://gepia.pku.cn/ ) and ONCOMINE ( https://www.oncomine.org/ ) were used to analyze PADI2 Gene Expression data. The survival curve for the PADI2 gene was generated by using the online Kaplan-Meier mapping site ( https://www.kmplot.com/ ). We conducted MTT assay, cloning formation assay and EdU cell proliferation assay to detect the cell activity of PADI2 knockdown A2780 and SKOV3 ovarian cancer cells treated with Olaparib. Cell migration and invasion were observed by would healing and transwell assay. The pathway changes after the treatment of PADI2 were detected by transcriptome sequencing and western blot. The role of PADI2 combined with Olaparib treatment in vivo was studied in nude mouse model bearing ovarian cancer tumor. RESULTS: We investigated the role of PADI2 on EOC in vitro and in vivo. PADI2 was upregulated in ovarian cancer samples and high PADI2 expression was correlated with poor outcome. Downregulating PADI2 suppressed colony formation, proliferation, migration and invasion of A2780 and SKOV3 cells. Furthermore, downregulating PADI2 and Olaparib combination treatment attenuated the viability, migration and invasion of A2780 and SKOV3 cells. We identified differentially expressed genes in A2780-shPADI2 and SKOV3-shPADI2 cell by transcriptome sequencing analysis and verified that downregulating PADI2 and Olaparib combination treatment suppresses EMT and JAK2/STAT3 signaling pathway in A2780 and SKOV3 cells in vitro and in vivo. CONCLUSIONS: Downregulation of PADI2 and Olaparib combination treatment attenuated the proliferation, migration and invasion of A2780 and SKOV3 cells by inhibiting the EMT through JAK2/STAT3 signaling pathway.

MiR-204 suppresses cell proliferation and promotes apoptosis in ovarian granulosa cells via targeting TPT1 in polycystic ovary syndrome.

MicroRNA (miR)-204 is known to be associated with several different diseases. Polycystic ovary syndrome (PCOS) has the highest incidence rate among the endocrine disorders in females between the ages of 18 and 44. We aimed to illustrate the miR-204 function in PCOS. MiR-204 expression levels in tissue and cell were examined through RT-qPCR. Colony formation assay and MTT assay were applied to detect the cell viability. Flow cytometry was employed to examine the apoptosis and cell cycle in cells. RNA binding protein immunoprecipitation assay and luciferase reporter assay were provided to demonstrate the direct interaction between translationally controlled tumor protein (TPT1) and miR-204. The expression of miR-204 was declined in KGN cells and ovarian cortex tissues of PCOS patients. MiR-204 enhanced the colony formation capacity and cell proliferation in KGN cells. Cell cycle and apoptosis were also influenced by miR-204. Since miR-204 has direct interaction with TPT1, TPT1 overexpression suppressed the miR-204-induced apoptosis and cell cycle alteration in KGN cells. MiR-204 inhibits the cell viability and induces apoptosis and cell cycle arrest by directly interacting with TPT1, indicating a role of miR-204 to be a potential target in the PCOS patients.

Kinetic resolution of ß-ketoesters with quaternary stereocenters via a carbene-catalyzed benzoin reaction.

Chiral ß-ketoesters bearing fully substituted carbon centers are important building blocks in organic synthesis. Mono-substituted ketoesters have been widely used to synthesize the above compounds through asymmetric additions or substitutions. The limitations of these protocols mainly exist in the substrate scopes, and α-methyl or α-fluoro-substituted ß-ketoesters or acetyl acetates are frequently used owing to their relatively higher reactivity. To break through this limitation, we employed N-heterocyclic carbene-catalyzed kinetic resolution to achieve the access to enantioenriched ß-ketoesters with quaternary stereocenters. Sterically more bulky groups such as benzyl, allyl, phenyl and cyclopropyl groups are all tolerated using this method.

[Role of TGF-ß1 in multi-drug resistance in small cell lung cancer and its clinical significance].

OBJECTIVE: To investigate the role of transforming growth factor ß1 (TGF-ß1) in multi-drug resistance in small cell lung cancer and its clinical significance.
 Methods: The mRNA and protein expressions of TGF-ß1 in H69 and H69AR cells were detected by real-time PCR and Western blot, respectively. After silence of TGF-ß1, the sensitivity of H69AR to drugs was detected by CCK8 assay. The expressions of TGF-ß1 in lung cancer and paracarcinoma tissues were examined by QRT-PCR and immunohistochemistry. The relationship of TGF-ß1 expression with clinical pathological features and prognosis of patients was studied.
 Results: Compared to H69, the mRNA and protein expressions of TGF-ß1 in H69AR cells were significantly increased by (5.93±0.47) and (8.49±1.92) folds, respectively (P<0.01). Transfection of TGF-ß1 siRNA resulted in a decrease of TGF-ß1 expression by 70.432% in H69AR cells (F=21.20, P<0.01) and an increase insensitivity to chemotherapeutic agents of H69AR cells (t=4.576, P<0.05). Compare with the paracarcinoma tissues, the expression of TGF-ß1 was significantly increased in small cell lung cancer tissues (t=13.925, P<0.01), which was closely related with clinical stage, chemosensitivity and overall survival (all P<0.05), but not related with gender, age (both P>0.05).
 Conclusion: TGF-ß1 is involved in the regulation of small cell lung cancer multidrug resistance, which may be a potential marker to evaluate the chemosensitivity and clinical prognostic for small cell lung cancer.

Dynamic Kinetic Resolution Enabled by Intramolecular Benzoin Reaction: Synthetic Applications and Mechanistic Insights.

The highly enantio-, diastereo-, and regioselective dynamic kinetic resolution of ß-ketoesters and 1,3-diketones was achieved via a chiral N-heterocyclic carbene catalyzed intramolecular cross-benzoin reaction. A variety of tetralone derivatives bearing two contiguous stereocenters and multiple functionalities were liberated in moderate to excellent yields and with high levels of stereoselectivity (>95% ee and >20:1 dr in most cases). In addition, the excellent regioselectivity control for aryl/alkyl 1,3-diketones, and the superior electronic differentiation of 1,3-diarylketones were highlighted. Moreover, a set of new mechanistic rationale that differs with the currently widely accepted understanding of intramolecular benzoin reactions was established to demonstrate the superior preference of benzoin over aldol transformation: (1) A coexistence of competitive aldol and benzoin reactions was detected, but a retro-aldol-irreversible benzoin process performs a vital role in the generation of predominant benzoin products. (2) The most essential role of an N-electron-withdrawing substituent in triazolium catalysts was revealed to be accelerating the rate of the benzoin transformation, rather than suppressing the aldol process through reducing the inherent basicity of the catalyst.

Asymmetric Desymmetrization of 1,3-Diketones via Intramolecular Benzoin Reaction.

A general method for the asymmetric desymmetrization of 1,3-diketone substrates via chiral N-heterocyclic carbene catalyzed intramolecular benzoin reactions was developed. Five- and six-membered cyclic ketones bearing two contiguous fully substituted stereocenters were generated with excellent diastereoselectivities and moderate to excellent enantioselectivities.

Grafting Poly(ethylene glycol) Onto Single-Walled Carbon Nanotubes by Living Anionic Ring-Opening Polymerization.

Recent years, many methods have been developed to widen the practical application of single-walled carbon nanotubes (SWCNTs). Among them, PEGylation is a general strategy to endow functionality, biocompatibility as well as its good solubility. In this paper, poly(ethylene glycol) (PEG) is successfully grafted onto SWCNTs through living anionic ring-opening polymerization of ethylene oxide (EO). By controlling the amount of monomer and initiator, a series of PEGylated SWCNTs with different PEG molecular weight and density are prepared. Then, the as-prepared SWCNTs have been verified by thermogravimetric analyses (TGA), Raman spectroscopy, Fourier transform infrared (FT-IR) spectroscopy, X-ray photoelectron spectroscopy (XPS). Finally, the protein resistance property of the PEGylated SWCNTs is investigated. It is found that these PEGylated SWCNTs have a good protein resistance property and the higher the content of PEG grafted on the SWCNTs, the less adsorption amount of BSA and the larger capacity to resist protein absorption. This work provides a novel method to prepare PEGylated SWCNTs.

The efficacy of the combination of venetoclax and hypomethylating agents versus HAG agents in patients with acute myeloid leukemia: a retrospective study.

OBJECTIVES: The purpose of this study was to compare the effectiveness of the combination of venetoclax and hypomethylating agents with the HAG regimen. METHODS: We studied 52 cases of newly diagnosed AML and 26 cases of relapsed refractory AML, (including AML patients with treatment-related and ELN-adverse risk disease (n = 50)). These patients were treated with venetoclax and hypomethylating agents and HAG regimens, respectively. RESULTS: Twenty-nine patients newly diagnosed with acute myeloid leukemia were treated with VEN-HMA (venetoclax-hypomethylating agent), while 23 patients were treated with HAG. The median age of the VEN-HMA group was 70 years, while the HAG group had a median age of 69 years. The VEN-HMA group achieved a significantly higher rate of complete remission (82.7%) compared to the cohort treated with the HAG regimen (21.7%) (P < 0.001). At the same time, the VEN-HMA group exhibited a significant survival advantage compared to the HAG treatment group(HR = 0.328, 95%CI: 0.158-0.683, P = 0.003).In patients with relapsed and refractory acute myeloid leukaemia, 43.8% of patients in the VEN-HMA treatment group achieved complete remission, which was similar to the 50% in the HAG treatment group (P > 0.99). The median overall survival was similar between the VEN-HMA and HAG groups, with 4 and 3.67 months, respectively (P = 0.290). CONCLUSIONS: In conclusion, our analyses indicated that VEN-HMA resulted in better therapeutic outcomes compared to HAG for newly diagnosed AML patients, with higher rates of complete remission and overall survival. In relapsed/refractory AML patients, there was no significant difference in the efficacy of the two treatments and further studies with larger sample sizes are warranted.

Efficacy and safety of immunosuppressive therapy combined with eltrombopag for severe aplastic anemia: a systematic review and meta-analysis.

BACKGROUND AND OBJECTIVE: Immunosuppressive therapy (IST) is the first choice for severe aplastic anemia (SAA) patients with hematopoietic stem cell transplantation (HSCT) limitation, and the main factor limiting its efficacy is too few residual hematopoietic stem/progenitor cells (HSPC). Eltrombopag (EPAG), as a small molecule thrombopoietin receptor agonist, can stimulate the proliferation of residual HSPC and restore the bone marrow hematopoietic function of patients. In recent years, many studies have observed the efficacy and safety of IST combined with EPAG in the treatment of SAA, but the results are still controversial. The aim of this study is to systematically evaluate the efficacy and safety of IST combined with or without EPGA in the treatment of SAA. METHODS: We conducted a systematic review of all relevant literature published up to January 19, 2024. Pooled odds ratio (OR) was calculated to compare the rates, along with 95% confidence intervals (CI) and p value to assess whether the results were statistically significant by Review Manager 5.4.1. The p values for the interactions between each subgroup were calculated by Stata 15.1. The Newcastle-Ottawa Scale and the Cochrane bias risk assessment tools were respectively used to evaluate the quality of the literature with cohort studies and randomized controlled trials. The Review Manager 5.4.1 and Stata 15.1 were used to assess bias risk and perform the meta-analysis. RESULTS: A total of 16 studies involving 2148 patients were included. The IST combined with the EPAG group had higher overall response rate (ORR) than the IST group at 3 months (pooled OR = 2.10, 95% CI 1.58-2.79, p < 0.00001) and 6 months (pooled OR = 2.13, 95% CI 1.60-2.83, p < 0.00001), but the difference between the two groups became statistically insignificant at 12 months (pooled OR = 1.13, 95% CI 0.75-1.72, p = 0.55). The results of complete response rate (CRR) (pooled OR at 3 months = 2.73, 95% CI 1.83-4.09, p < 0.00001, 6 months = 2.76, 95% CI 2.08-3.67, p < 0.00001 and 12 months = 1.38, 95% CI 0.85-2.23, p = 0.19) were similar to ORR. Compared with the IST group, the IST combined with the EPAG group had better overall survival rate (OSR) (pooled OR = 1.70, 95% CI 1.15-2.51, p = 0.008), but there were no statistically significant differences in event-free survival rate (EFSR) (pooled OR = 1.40, 95% CI 0.93-2.13, p = 0.11), clonal evolution rate (pooled OR = 0.68, 95% CI 0.46-1.00, p = 0.05) and other adverse events between the two groups. The results of subgroup analysis showed that different ages were a source of heterogeneity, but different study types and different follow-up times were not. Moreover, all p-values for the interactions were greater than 0.05, suggesting that the treatment effect was not influenced by subgroup characteristics. CONCLUSION: EPAG added to IST enables patients to achieve earlier and faster hematologic responses with a higher rate of complete response. Although it had no effect on overall EFSR, it improved OSR and did not increase the incidence of clonal evolution and other adverse events.

A case report: Nonsecretory multiple myeloma presenting with bone pain.

RATIONALE: Nonsecretory multiple myeloma (NSMM) is a rare subtype of multiple myelom, occurring in 1% to 2% of multiple myelom and characterized by the inability of clonal plasma cells to synthesize or secrete immunoglobulins. We describe a 71-year-old male patient who began with bone pain and was referred to hospital several times, but was not properly diagnosed and effectively treated. PATIENT CONCERNS: A 71-year-old male patient visited our hematology department, complaining of lumbago for 1 year and back pain for half a year. DIAGNOSES: Low-dose whole-body bone computed tomography: multiple bone destruction of the sternum, ribs, multiple vertebrae and accessories of the spine, pelvis, bilateral humerus, and proximal femur. Monoclonal plasma cells accounted for 17.5% of nuclear cells in bone marrow puncture smear. Fluorescence in situ hybridization detected amplification of CKS1B (1q21) gene. Immunofixation electrophoresis negative. About 10.72% of monoclonal plasma cells were detected by flow cytometry. Finally, he was diagnosed with NSMM. INTERVENTIONS: The patients received VCD chemotherapy (bortezomib 1.3 mg/m2, d1, d4, d8, d11; cyclophosphamide 300 mg/m2, d1-2, d8-9; dexamethasone sodium phosphate 20 mg, d1-2, d4-5, d8-9, d11-12, once every 21 days). OUTCOMES: After 2 cycles of VCD treatment, the symptoms of bone pain were significantly relieved, and the efficacy was evaluated as partial response. Follow-up chemotherapy will continue to be completed on schedule. We will continue to follow up to further evaluate the overall survival and progression-free survival. LESSONS: This case shows that NSMM is easily missed or misdiagnosed.

Structurally disordered MoSe2 with rich 1T phase as a universal platform for enhanced photocatalytic hydrogen production.

The improvement of surface reactivity in noble-metal-free cocatalysts is crucial for the development of efficient and cost-effective photocatalytic systems. However, the influence of crystallinity on catalytic efficacy has received limited attention. Herein, we report the utilization of structurally disordered MoSe2 with abundant 1T phase as a versatile cocatalyst for photocatalytic hydrogen evolution. Using MoSe2/carbon nitride (CN) hybrids as a case study, it is demonstrated that amorphous MoSe2 significantly enhances the hydrogen evolution rate of CN, achieving up to 11.37 µmol h-1, surpassing both low crystallinity (8.24 µmol h-1) and high crystallinity MoSe2 (3.86 µmol h-1). Experimental analysis indicates that the disordered structure of amorphous MoSe2, characterized by coordination-unsaturated surface sites and a rich 1T phase with abundant active sites at the basal plane, predominantly facilitates the conversion of surface-bound protons to hydrogen. Conversely, the heightened charge transfer capacity of the highly crystalline counterpart plays a minor role in enhancing practical catalytic performance. This approach is applicable for enhancing the photocatalytic hydrogen evolution performance of various semiconducting photocatalysts, including CdS, TiO2, and ZnIn2S4, thereby offering novel insights into the advancement of high-performance non-precious catalysts through phase engineering.

A skeletal randomization strategy for high-performance quinoidal-aromatic polymers.

Enhancing the solution-processability of conjugated polymers (CPs) without diminishing their thin-film crystallinity is crucial for optimizing charge transport in organic field-effect transistors (OFETs). However, this presents a classic "Goldilocks zone" dilemma, as conventional solubility-tuning methods for CPs typically yield an inverse correlation between solubility and crystallinity. To address this fundamental issue, a straightforward skeletal randomization strategy is implemented to construct a quinoid-donor conjugated polymer, PA4T-Ra, that contains para-azaquinodimethane (p-AQM) and oligothiophenes as repeat units. A systematic study is conducted to contrast its properties against polymer homologues constructed following conventional solubility-tuning strategies. An unusually concurrent improvement of solubility and crystallinity is realized in the random polymer PA4T-Ra, which shows moderate polymer chain aggregation, the highest crystallinity and the least lattice disorder. Consequently, PA4T-Ra-based OFETs, fabricated under ambient air conditions, deliver an excellent hole mobility of 3.11 cm2 V-1 s-1, which is about 30 times higher than that of the other homologues and ranks among the highest for quinoidal CPs. These findings debunk the prevalent assumption that a random polymer backbone sequence results in decreased crystallinity. The considerable advantages of the skeletal randomization strategy illuminate new possibilities for the control of polymer aggregation and future design of high-performance CPs, potentially accelerating the development and commercialization of organic electronics.

A Three-in-One Hybrid Strategy for High-Performance Semiconducting Polymers Processed from Anisole.

The development of semiconducting polymers with good processability in green solvents and competitive electrical performance is essential for realizing sustainable large-scale manufacturing and commercialization of organic electronics. A major obstacle is the processability-performance dichotomy that is dictated by the lack of ideal building blocks with balanced polarity, solubility, electronic structures, and molecular conformation. Herein, through the integration of donor, quinoid and acceptor units, an unprecedented building block, namely TQBT, is introduced for constructing a serial of conjugated polymers. The TQBT, distinct in non-symmetric structure and high dipole moment, imparts enhanced solubility in anisole-a green solvent-to the polymer TQBT-T. Furthermore, PTQBT-T possess a highly rigid and planar backbone owing to the nearly coplanar geometry and quinoidal nature of TQBT, resulting in strong aggregation in solution and localized aggregates in film. Remarkably, PTQBT-T films spuncast from anisole exhibit a hole mobility of 2.30 cm2 V-1 s-1, which is record high for green solvent-processable semiconducting polymers via spin-coating, together with commendable operational and storage stability. The hybrid building block emerges as a pioneering electroactive unit, shedding light on future design strategies in high-performance semiconducting polymers compatible with green processing and marking a significant stride towards ecofriendly organic electronics.

PI3K is required for the physical interaction and functional inhibition of NF-κB by ß-catenin in colorectal cancer cells.

Activation of ß-catenin and PI3K pathways are crucial for the oncogenesis of colorectal cancer (CRC). It remains controversial whether these two pathways function independently or cooperatively in the development and progression of CRC. We showed previously that ß-catenin inhibited NF-κB activation by interacting with p65 and this inhibitory interaction involved an unidentified cellular protein. In this study, we found that the PI3K effect on NF-κB activity is dependent on the level of ß-catenin in CRC cells. PI3K promoted NF-κB activity in the ß-catenin-low RKO cells; whereas it inhibited NF-κB activity in the ß-catenin-high HCT116, DLD-1, and SW480 cells. We showed that PI3K is required for the physical interaction and functional inhibition of NF-κB by ß-catenin. Inhibition of PI3K released NF-κB suppression in ß-catenin-high CRC cells, which conferred these cells with susceptibility to TNFα- and Fas-induced apoptosis. This is consistent with the observation showing that the level of ß-catenin and activated Akt are both inversely correlated with the expression of Fas, a downstream target of NF-κB, in CRC specimens. Mechanistically, the PI3K subunit p85 formed a complex with ß-catenin and NF-κB. Inhibition of PI3K disrupted the complex formation, leading to NF-κB activation. Our study not only provides new insight into the cross-talk among PI3K, ß-catenin and NF-κB signaling pathways but also indicates that targeting PI3K may yield therapeutic efficacy in treating ß-catenin-high CRC.

Dual-responsive capsules with tunable low critical solution temperatures and their loading and release behavior.

Dual-responsive capsules sensitive to pH and temperature changes were successfully prepared by grafting random copolymer brushes of 2-(2-methoxyethoxy)ethyl methacrylate (MEO2MA) and oligo(ethylene glycol) methacrylate (OEGMA) from polydopamine (Pdop)-coated SiO2 via a surface-initiated atom-transfer radical polymerization (SI-ATRP) method with subsequent removal of the SiO2 core. The uptake and release properties of the resulting capsules are highly affected by changes in the pH values and temperature of the solution. The capsules can take up cationic dye rhodamine 6G (Rh6G) at high pH and T < LCST but not at low pH and T > LCST. In contrast, the capsules can release Rh6G at pH < 7 and temperature below the LCST, but release is less efficient under the opposite conditions. This dual-responsive property was also observed for the anionic dye methyl orange.

Photoinduced Disulfide-Catalyzed Intramolecular Anti-Markovnikov Hydroamination through in Situ N-S Species.

The photoinduced anti-Markovnikov hydroamination of olefins typically required photocatalysts with a high oxidative ability to initiate the single-electron process. Herein, we alternatively utilize bis(2,4,6-triisopropylphenyl) disulfide, an inexpensive reagent with relatively low oxidative ability, as a photo and hydrogen atom transfer catalyst to achieve intramolecular hydroamination. The mechanistic studies as well as the DFT calculations are consistent with a novel process involving N-centered radical generation through the homolysis of the in situ formed N-S species and subsequent cyclization. An array of diverse nitrogen-containing cycles could be obtained.

General Anti-Markovnikov Hydrophosphinylation of Olefins Using Disulfide as the Photocatalyst and a Hydrogen Atom Shuttle.

The photoinduced radical-based hydrophosphinylation suffered from substrate scope limitation due to the highly electrophilic property of the P(O) radical. Herein, we report an efficient catalytic system for the intermolecular anti-Markovnikov hydrophosphinylation of olefins using disulfide as a photocatalyst and also a hydrogen atom shuttle. This metal-free, base-free, and redox-neutral condition allowed the alkenes with diverse electronic properties to proceed with the anti-Markovnikov P-H addition efficiently. A plausible mechanism involving the HAT process between ArS• and P(O)-H was proposed.

Recent Advances in Phase-Engineered Photocatalysts: Classification and Diversified Applications.

Phase engineering is an emerging strategy for tuning the electronic states and catalytic functions of nanomaterials. Great interest has recently been captured by phase-engineered photocatalysts, including the unconventional phase, amorphous phase, and heterophase. Phase engineering of photocatalytic materials (including semiconductors and cocatalysts) can effectively affect the light absorption range, charge separation efficiency, or surface redox reactivity, resulting in different catalytic behavior. The applications for phase-engineered photocatalysts are widely reported, for example, hydrogen evolution, oxygen evolution, CO2 reduction, and organic pollutant removal. This review will firstly provide a critical insight into the classification of phase engineering for photocatalysis. Then, the state-of-the-art development of phase engineering toward photocatalytic reactions will be presented, focusing on the synthesis and characterization methodologies for unique phase structure and the correlation between phase structure and photocatalytic performance. Finally, personal understanding of the current opportunities and challenges of phase engineering for photocatalysis will also be provided.

The uncharacterized transcript KIAA0930 confers a cachexic phenotype on cancer cells.

Patients with cancer cachexia have a poor prognosis and impaired quality of life. Numerous studies using preclinical models have shown that inflammatory cytokines play an important role in the development of cancer cachexia; however, no clinical trial targeting cytokines has been successful. Therefore, it is essential to identify molecular mechanisms to develop anti-cachexia therapies. Here we identified the uncharacterized transcript KIAA0930 as a candidate cachexic factor based on analyses of microarray datasets and an in vitro muscle atrophy assay. While conditioned media from pancreatic, colorectal, gastric, and tongue cancer cells caused muscle atrophy in vitro, conditioned medium from KIAA0930 knockdown cells did not. The PANC-1 orthotopic xenograft study showed that the tibialis anterior muscle weight and cross-sectional area were increased in mice bearing KIAA0930 knockdown cells compared to control mice. Interestingly, KIAA0930 knockdown did not cause consistent changes in the secretion of inflammatory cytokines/chemokines from a variety of cancer cell lines. An initial characterization experiment showed that KIAA0930 is localized in the cytosol and not secreted from cells. These data suggest that the action of KIAA0930 is independent of the expression of cytokines/chemokines and that KIAA0930 could be a novel therapeutic target for cachexia.