A combined network pharmacology and molecular biology approach to investigate the potential mechanisms of G-M6 on ovarian cancer.

Ginsenoside 3ß,12ß,21α,22ß-Hydroxy-24-norolean-12-ene (G-M6), a phase I metabolite of anti-tumor medication 20(R)-25-methoxyl-dammarane-3ß,12ß,20-triol (AD-1), beats the parent drug in anti-ovarian cancer efficacy. The mechanism of action for ovarian cancer, however, is uncertain. Using network pharmacology, human ovarian cancer cells and nude mouse ovarian cancer xenotransplantation model, the anti-ovarian cancer mechanism of G-M6 was preliminarily explored in this study. The PPAR signal pathway is the key signal pathway of the G-M6 anti-ovarian cancer mechanism, according to data mining and network analysis. Docking tests demonstrated that the bioactive chemical G-M6 was capable of forming a stable bond with the PPARγ target protein capsule. Using human ovarian cancer cells and xenograft model of ovarian cancer to evaluate the anticancer activity of G-M6. The IC50 value of G-M6 was 5.83±0.36, lower than AD-1 and Gemcitabine. The tumor weight of the RSG 80 mg/kg group (C), G-M6 80 mg/kg group (I), and RSG 80 mg/kg + G-M6 80 mg/kg group (J) after the intervention was as follows: C < I < J. The tumor inhibition rates of groups C, I, and J were 28.6%, 88.7%, and 92.6%, respectively. When RSG and G-M6 are combined to treat ovarian cancer, q = 1.00 is calculated according to King's formula, which indicates that RSG and G-M6 have additive effects. Its molecular mechanism may involve the up-regulation of PPARγ and Bcl-2 protein expressions, and the down-regulation of Bax, Cytochrome C (Cyt. C), Caspase-3, and Caspase-9 protein expressions. These findings serve as a reference for further research into the processes behind ginsenoside G-M6's ovarian cancer therapy.

Paeonol regulates NLRP3 inflammasomes and pyroptosis to alleviate spinal cord injury of rat.

BACKGROUND: Spinal cord injury (SCI) is a life-threatening traumatic disorder. Paeonol has been confirmed to be involved in a variety of diseases. The purpose of this study is to investigate the role of paeonol on SCI progression. METHODS: Sprague Dawley (SD) rat was used for the establishment of SCI model to explore the anti-inflammation, anti-oxidation, and neuroprotective effects of paeonol (60 mg/kg) on SCI in vivo. For in vitro study, mouse primary microglial cells (BV-2) were induced by lipopolysaccharide (LPS)/adenosine triphosphate (ATP) treatment. The effect of paeonol on the polarization of LPS/ATP-induced BV-2 cells was determined by detection the expression inducible nitric oxide synthase (iNOS), tumour necrosis factor alpha (TNF-α), arginase-1 (Arg-1), and interleukin (IL)-10 using qRT-PCR. ELISA was used to assess the levels of IL-1ß, IL-18, TNF-α, malondialdehyde (MDA), and glutathione (GSH). Western blotting was conducted to determine the levels of NLRP3 inflammasomes and TLR4/MyD88/NF-κB (p65) pathway proteins. RESULTS: Paeonol promoted the recovery of locomotion function and spinal cord structure, and decreased spinal cord water content in rats following SCI. Meanwhile, paeonol reduced the levels of apoptosis-associated speck-like protein (ASC), NLRP3, active caspase 1 and N-gasdermin D (N-GSDMD), repressed the contents of IL-1ß, IL-18, TNF-α and MDA, and elevated GSH level. In vitro, paeonol exerted similarly inhibiting effects on pyroptosis and inflammation. Meanwhile, paeonol promoted BV-2 cells M2 polarization. In addition, paeonol also inactivated the expression of TLR4/MyD88/NF-κB (p65) pathway. CONCLUSION: Paeonol may regulate NLRP3 inflammasomes and pyroptosis to alleviate SCI, pointing out the potential for treating SCI in clinic.

Experimental Demonstration of Remotely Creating Wigner Negativity via Quantum Steering.

Non-Gaussian states with Wigner negativity are of particular interest in quantum technology due to their potential applications in quantum computing and quantum metrology. However, how to create such states at a remote location remains a challenge, which is important for efficiently distributing quantum resource between distant nodes in a network. Here, we experimentally prepare an optical non-Gaussian state with negative Wigner function at a remote node via local non-Gaussian operation and shared Gaussian entangled state existing quantum steering. By performing photon subtraction on one mode, Wigner negativity is created in the remote target mode. We show that the Wigner negativity is sensitive to loss on the target mode, but robust to loss on the mode performing photon subtraction. This experiment confirms the connection between the remotely created Wigner negativity and quantum steering. As an application, we present that the generated non-Gaussian state exhibits metrological power in quantum phase estimation.

Ultrafast Tracking of a Single Live Virion During the Invagination of a Cell Membrane.

The first step in most viral infections is the penetration of the cell membrane via endocytosis. However, the underlying mechanism of this important process has not been quantitatively characterized; for example, the velocity and force of a single virion during invagination remain unknown. Here, the endocytosis of a single live virion (Singapore grouper iridovirus, SGIV) through the apical membranes of a host cell is monitored by developing and using a novel ultrafast (at the microsecond level) tracking technique: force tracing. For the first time, these results unambiguously reveal that the maximum velocity during the cell entry of a single SGIV by membrane invagination is approximately 200 nm s(-1), the endocytic force is approximately 60.8 ± 18.5 pN, and the binding energy density increases with the engulfment depth. This report utilizing high temporospatial resolution (subnanometer and microsecond levels) approaches provides new insight into the dynamic process of viral infection via endocytosis and the mechanism of membrane invagination at the single-particle level.

Multiple chiroptical switches and logic circuit based on salicyl‒ imine‒chitosan hydrogel.

A chitosan-based chiral hydrogel was fabricated by grafting achiral salicylaldehyde (SA) on chitosan chains, followed by supramolecular assembly (CS-SA hydrogel hereafter). The structures and properties of the CS-SA hydrogel were characterized and investigated. The results indicated that the swelling ability of the CS-SA hydrogel depended on the medium pH and crosslinking degree. Circular dichroism measurements revealed that the chiral information of the chitosan was successfully transcribed to the achiral salicylic chromophores through imine bonds. Chiroptical switches based on acid-base responses of the imine bond and the OH fragment of SA and the swelling properties of the CS-SA hydrogel were fabricated, which is first reported for a chitosan-based hydrogel. In addition, a gel film showed good fatigue resistance under external stimuli. IMPLICATION, INHIBIT, and PASS logic gates and a logic circuit based on the chiroptical switches were successfully designed. This study suggests a new method of constructing biobased chiral functional materials.

Silencing of the Long Non-Coding RNA TTN-AS1 Attenuates the Malignant Progression of Osteosarcoma Cells by Regulating the miR-16-1-3p/TFAP4 Axis.

OBJECTIVES: Osteosarcoma (OS) is a type of bone malignancy. This study attempted to explore the effect of long non-coding RNA TTN-AS1 (TTN-AS1) on OS and to determine its molecular mechanisms. METHODS: The expression of TTN-AS1, microRNA-16-1-3p (miR-16-1-3p), and transcription factor activating enhancer binding protein 4 (TFAP4) in OS was assessed using qRT-PCR. The OS cell proliferation, migration, and invasion were measured using 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), wound-healing, and transwell assays. N-cadherin and MMP-2 protein level was determined with western blot. Interactions between TTN-AS1 and miR-16-1-3p or TFAP4 and miR-16-1-3p were confirmed using the dual-luciferase reporter assay. Additionally, an OS xenograft tumor model was constructed to assess the effect of TTN-AS1 on tumor growth. RESULTS: TTN-AS1 and TFAP4 expression was increased in OS, while miR-16-1-3p expression was decreased. TTN-AS1 silencing restrained OS cell proliferation, migration, invasion, N-cadherin and MMP-2 protein expression, and hindered tumor growth. MiR-16-1-3p overexpression retarded the malignant behavior of OS cells. TTN-AS1 played a carcinostatic role by down-regulating miR-16-1-3p in the OS cells. Moreover, miR-16-1-3p inhibition or TFAP4 elevation weakened the suppressive effect of TTN-AS1 silencing on OS cell tumor progression. CONCLUSION: TTN-AS1 promoted the proliferation, migration, invasion, and epithelial-mesenchymal transition (EMT) of OS cells via mediating the miR-16-1-3p/TFAP4 axis. TTN-AS1 may be a critical target for improving OS.

Endovascular Perforation Model for Subarachnoid Hemorrhage Combined with Magnetic Resonance Imaging (MRI).

The endovascular filament perforation model to mimic subarachnoid hemorrhage (SAH) is a commonly used model - however, the technique can cause a high mortality rate as well as an uncontrollable volume of SAH and other intracranial complications such as stroke or intracranial hemorrhage. In this protocol, a standardized SAH mouse model is presented, induced by endovascular filament perforation, combined with magnetic resonance imaging (MRI) 24 h after operation to ensure the correct bleeding site and exclude other relevant intracranial pathologies. Briefly, C57BL/6J mice are anesthetized with an intraperitoneal ketamine/xylazine (70 mg/16 mg/kg body weight) injection and placed in a supine position. After midline neck incision, the common carotid artery (CCA) and carotid bifurcation are exposed, and a 5-0 non-absorbable monofilament polypropylene suture is inserted in a retrograde fashion into the external carotid artery (ECA) and advanced into the common carotid artery. Then, the filament is invaginated into the internal carotid artery (ICA) and pushed forward to perforate the anterior cerebral artery (ACA). After recovery from surgery, mice undergo a 7.0 T MRI 24 h later. The volume of bleeding can be quantified and graded via postoperative MRI, enabling a robust experimental SAH group with the option to perform further subgroup analyses based on blood quantity.

RNase A Inhibits Formation of Neutrophil Extracellular Traps in Subarachnoid Hemorrhage.

Background: Subarachnoid hemorrhage (SAH) caused by rupture of an intracranial aneurysm, is a life-threatening emergency that is associated with substantial morbidity and mortality. Emerging evidence suggests involvement of the innate immune response in secondary brain injury, and a potential role of neutrophil extracellular traps (NETs) for SAH-associated neuroinflammation. In this study, we investigated the spatiotemporal patterns of NETs in SAH and the potential role of the RNase A (the bovine equivalent to human RNase 1) application on NET burden. Methods: A total number of n=81 male C57Bl/6 mice were operated utilizing a filament perforation model to induce SAH, and Sham operation was performed for the corresponding control groups. To confirm the bleeding and exclude stroke and intracerebral hemorrhage, the animals received MRI after 24h. Mice were treated with intravenous injection of RNase A (42µg/kg body weight) or saline solution for the control groups, respectively. Quadruple-immunofluorescence (IF) staining for cell nuclei (DAPI), F-actin (phalloidin), citrullinated H3, and neurons (NeuN) was analyzed by confocal imaging and used to quantify NET abundance in the subarachnoid space (SAS) and brain parenchyma. To quantify NETs in human SAH patients, cerebrospinal spinal fluid (CSF) and blood samples from day 1, 2, 7, and 14 after bleeding onset were analyzed for double-stranded DNA (dsDNA) via Sytox Green. Results: Neutrophil extracellular traps are released upon subarachnoid hemorrhage in the SAS on the ipsilateral bleeding site 24h after ictus. Over time, NETs showed progressive increase in the parenchyma on both ipsi- and contralateral site, peaking on day 14 in periventricular localization. In CSF and blood samples of patients with aneurysmal SAH, NETs also increased gradually over time with a peak on day 7. RNase application significantly reduced NET accumulation in basal, cortical, and periventricular areas. Conclusion: Neutrophil extracellular trap formation following SAH originates in the ipsilateral SAS of the bleeding site and spreads gradually over time to basal, cortical, and periventricular areas in the parenchyma within 14days. Intravenous RNase application abrogates NET burden significantly in the brain parenchyma, underpinning a potential role in modulation of the innate immune activation after SAH.

A generalized multipath delayed-choice experiment on a large-scale quantum nanophotonic chip.

Bohr's complementarity is one central tenet of quantum physics. The paradoxical wave-particle duality of quantum matters and photons has been tested in Young's double-slit (double-path) interferometers. The object exclusively exhibits wave and particle nature, depending measurement apparatus that can be delayed chosen to rule out too-naive interpretations of quantum complementarity. All experiments to date have been implemented in the double-path framework, while it is of fundamental interest to study complementarity in multipath interferometric systems. Here, we demonstrate generalized multipath wave-particle duality in a quantum delayed-choice experiment, implemented by large-scale silicon-integrated multipath interferometers. Single-photon displays sophisticated transitions between wave and particle characters, determined by the choice of quantum-controlled generalized Hadamard operations. We characterise particle-nature by multimode which-path information and wave-nature by multipath coherence of interference, and demonstrate the generalisation of Bohr's multipath duality relation. Our work provides deep insights into multidimensional quantum physics and benchmarks controllability of integrated photonic quantum technology.

LINC00662 Long Non-Coding RNA Knockdown Attenuates the Proliferation, Migration, and Invasion of Osteosarcoma Cells by Regulating the microRNA-15a-5p/Notch2 Axis.

PURPOSE: Osteosarcoma (OS) is a frequently occurring malignancy in children and adolescents. In this study, we aimed to investigate the effects of the long non-coding RNA (lncRNA) LINC00662 (LINC00662) in OS and the underlying molecular mechanism. METHODS: The expression of LINC00662, microRNA-15a-5p (miR-15a-5p), and Notch2 in OS was detected by quantitative real-time polymerase chain reaction (qRT-PCR). The proliferation, migration, and invasion of OS cells were analyzed by 3-(4,5-Dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT), wound-healing, and transwell assay. The interactions among LINC00662, miR-15a-5p, and Notch2 were determined by dual-luciferase reporter assays. A tumor xenograft model was established in mice for evaluating tumor growth in vivo. RESULTS: The expression of LINC00662 and Notch2 was found to be upregulated in OS, but the expression of miR-15a-5p was downregulated. The results demonstrated that LINC00662 knockdown attenuated the proliferation, migration, and invasion of OS cells and suppressed tumor growth in mice. The study further demonstrated that LINC00662 directly interacted with miR-15a-5p, and that Notch2 was a target of miR-15a-5p. The inhibition of miR-15a-5p or Notch2 overexpression markedly reversed the suppressive effect of sh-LINC00662 on the proliferation, migration, and invasion of OS cells. CONCLUSION: The study demonstrated that LINC00662 could be a potential biomarker for OS therapy, and LINC00662 knockdown suppressed the proliferation, migration, and invasion of OS cells by regulating the miR-15a-5p/Notch2 axis.

Green tea polyphenols protect PC12 cells against H2O2-induced damages by upregulating lncRNA MALAT1.

It is of significance to alleviate oxidative damages for the treatment of spinal cord injury (SCI). Studies have ascertained that green tea polyphenols (GTPs) exert protective activities against oxidative damages. In this study, we aimed to investigate the protective effects of GTP against H2O2-caused injuries in PC12 cells as well as the molecular underpinnings associated with long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1). PC12 cells were preincubated with GTP prior to H2O2 stimulation. Furthermore, MALAT1-deficient PC12 cells were constructed by transfection and identified by quantitative real-time polymerase chain reaction (qRT-PCR) assay. Next, viability and apoptosis were detected by cell counting kit-8 and flow cytometry, respectively. Meanwhile, Western blot assay was carried out to monitor the expression alteration of proteins associated with apoptosis (Bcl-2, Bax, pro-Caspase-3/9, and cleaved Caspase-3/9) and autophagy (microtubule-associated protein 1 light chain 3 (LC3)-II, LC3-I, Beclin-1, and p62). Moreover, we examined the expression of ß-catenin and dissected the phosphorylation of phosphatidylinositol 3'-kinase (PI3K) and protein kinase B (AKT). We found that H2O2 decreased the viability of PC12 cells while initiated apoptosis and autophagy processes. GTP-preincubated PC12 cells maintained the viability and resisted the apoptosis and autophagy induced by H2O2. Pointedly, GTP-pretreated PC12 cells showed an increase in MALAT1 after H2O2 stimulation. Of note, the protective effects of GTP were buffered in MALAT1-deficient cells in response to H2O2. The expression of ß-catenin and phosphorylation of PI3K and AKT were upregulated by GTP, while MALAT1 knockdown led to opposite results. To sum up, GTP protected PC12 cells from H2O2-induced damages by the upregulation of MALAT1. This process might be through activating Wnt/ß-catenin and PI3K/AKT signal pathways.

Genome-wide identification of epithelial-mesenchymal transition-associated microRNAs reveals novel targets for glioblastoma therapy.

MicroRNAs (miRNA) regulate a number of cellular processes. Recent studies have indicated that these molecules function in the epithelial-mesenchymal transition (EMT). However, the crucial systematic role of EMT and miRNAs together in glioblastoma (GBM) remains poorly understood. The present study demonstrated that EMT was closely associated with malignant progression and clinical outcome using three independent glioma databases (GSE16011, Rembrandt and The Cancer Genome Atlas). Furthermore, integrated analysis of miRNAs and mRNA profiling in 491 GBM samples revealed an EMT biological process associated with an miRNA profile (19 positively and 18 negatively correlated miRNAs). Among these miRNAs, miR-95 and miR-223 indicated a high level of functional validation, reflecting their positive correlation with EMT. Additionally, the upregulation of miR-95, which was negatively correlated with EMT, inhibited cellular invasion in glioma U251 and LN229 cells and decreased the expression of the mesenchymal marker N-catenin, whereas an miRNA positively correlated with EMT, miR-223, exhibited the opposite effect. Therefore, the results of the present study could further enhance the current understanding of the functions of miRNAs in GBM, indicating that the EMT-specific miRNA signature may represent a novel target for GBM therapy.

Percutaneous fibrin glue therapy for meningeal cysts of the sacral spine with or without aspiration of the cerebrospinal fluid.

OBJECT: The authors assessed the efficacy of computed tomography (CT)-guided percutaneous injection of fibrin glue to treat meningeal cysts of the sacral spine in patients with back pain, and evaluated the necessity for cerebrospinal fluid (CSF) aspiration before glue injection. METHODS: Of the 31 patients in this study, 15 underwent injection of fibrin glue under CT guidance after aspiration of more than 15 ml of CSF (Group A), and 16 patients were treated with the glue but without CSF aspiration (Group B). Clinical results were evaluated after an average of 23 months of follow-up, and changes on the imaging studies were also evaluated. The clinical outcome and postoperative complications were analyzed. RESULTS: All 31 patients experienced resolution or marked improvement of symptoms for as long as 28 months after fibrin glue therapy. No patient experienced recurrence of symptoms during the follow-up interval. The postoperative pain relief was statistically significant (p < 0.001) according to evaluations in which a 100-mm visual analog pain scale was used. There were no statistical differences between the two groups (p > 0.05). CONCLUSIONS: Percutaneous CT-guided fibrin glue therapy for sacral arachnoid cysts may be a definitive therapy. It is unnecessary to aspirate the CSF before injection of the fibrin glue.

The Process of Wrapping Virus Revealed by a Force Tracing Technique and Simulations.

Viral entry into the host cell is the first step of virus infection; however, its dynamic process via endocytosis remains largely elusive. Here, the force tracing technique and single particle simulation are combined to investigate the invagination of single human enterovirus 71 (HEV71, a positive single-stranded RNA virus that is associated with hand, foot, and mouth disease) via cell membranes during its host cell entry. The experimental results reveal that the HEV71 invaginates in membrane vesicles at a force of 58 ± 16 pN, a duration time of 278 ± 68 ms. The simulation further shows that the virus can reach a partially wrapped state very fast, then the upper surface of the virus is covered by the membrane traveling over a long period of time. Combining the experiment with the simulation, the mechanism of membrane wrapping of virus is uncovered, which provides new insights into how the cell is operated to initiate the endocytosis of virus.

An emerging function of circRNA-miRNAs-mRNA axis in human diseases.

Circular RNAs (circRNAs), a novel class of long noncoding RNAs, are characterized by a covalently closed continuous loop without 5' or 3' polarities structure and have been widely found in thousands of lives including plants, animals and human beings. Utilizing the high-throughput RNA sequencing (RNA-seq) technology, recent findings have indicated thata great deal of circRNAs, which are endogenous, stable, widely expressed in mammalian cells, often exhibit cell type-specific, tissue-specific or developmental-stage-specific expression. Evidences are arising that some circRNAs might regulate microRNA (miRNA) function as microRNA sponges and play a significant role in transcriptional control. circRNAs associate with related miRNAs and the circRNA-miRNA axes are involved in a serious of disease pathways such as apoptosis, vascularization, invasion and metastasis. In this review, we generalize and analyse the aspects including synthesis, characteristics, classification, and several regulatory functions of circRNAs and highlight the association between circRNAs dysregulation by circRNA-miRNA-mRNA axis and sorts of diseases including cancer- related and non-cancer diseases."

Antiviral activity of chemical compound isolated from Artemisia morrisonensis against hepatitis B virus in vitro.

The compound p-hydroxyacetophenone (PHAP) isolated from Artemisia morrisonensis was found to have potential anti-HBV effects in HepG2 2.2.15 cells. We clarified its antiviral mode further and HBV-transfected Huh7 cells were used as the platform. During viral gene expression, treatment with PHAP had no apparent effects on the viral precore/pregenomic RNA. However, the 2.4-kb preS RNA of viral surface gene increased significantly relative to the 2.1-kb S RNA with PHAP. Promoter activity analysis demonstrated that PHAP had a potent effect on augmenting the viral preS promoter activity. The subsequent increase in the large surface protein and induce endoplasmic reticular (ER) stress has been reported previously. Interestingly, PHAP specifically reduced ER stress related GRP78 RNA/protein levels, but not those of GRP94, in treated Huh7 cells while PHAP also led to the significant intracellular accumulation of virus. Moreover, treatment with the ER chaperone inducer thapsigargin relieved the inhibitory effect of PHAP based on the supernatant HBV DNA levels of HBV-expressed cells. In conclusion, this study suggests that the mechanism of HBV inhibition by PHAP might involve the regulation of viral surface gene expression and block virion secretion by interference with the ER stress signaling pathway.

Studying the nucleated mammalian cell membrane by single molecule approaches.

The cell membrane plays a key role in compartmentalization, nutrient transportation and signal transduction, while the pattern of protein distribution at both cytoplasmic and ectoplasmic sides of the cell membrane remains elusive. Using a combination of single-molecule techniques, including atomic force microscopy (AFM), single molecule force spectroscopy (SMFS) and stochastic optical reconstruction microscopy (STORM), to study the structure of nucleated cell membranes, we found that (1) proteins at the ectoplasmic side of the cell membrane form a dense protein layer (4 nm) on top of a lipid bilayer; (2) proteins aggregate to form islands evenly dispersed at the cytoplasmic side of the cell membrane with a height of about 10-12 nm; (3) cholesterol-enriched domains exist within the cell membrane; (4) carbohydrates stay in microdomains at the ectoplasmic side; and (5) exposed amino groups are asymmetrically distributed on both sides. Based on these observations, we proposed a Protein Layer-Lipid-Protein Island (PLLPI) model, to provide a better understanding of cell membrane structure, membrane trafficking and viral fusion mechanisms.

Detection of carbohydrates on the surface of cancer and normal cells by topography and recognition imaging.

Galactose was detected and localized on the surface of cancer and normal cells by topography and recognition imaging at the single molecular level. There are more galactoses on cancer cells than on normal cells. The stability of galactose-lectin on cancer cells is much lower than that on normal cells.

High-efficiency localization of Na(+)-K(+) ATPases on the cytoplasmic side by direct stochastic optical reconstruction microscopy.

We describe a concise and effective strategy towards precisely mapping Na(+)-K(+) ATPases on the cytoplasmic side of cell membranes by direct stochastic optical reconstruction microscopy (dSTORM). We found that most Na(+)-K(+) ATPases are localized in different sizes of clusters on human red blood cell (hRBC) membranes, revealed by Ripley's K-function analysis. Further evidence that cholesterol depletion causes the dispersion of Na(+)-K(+) ATPase clusters indicates that such clusters could be localized in cholesterol-enriched domains. Our results suggest that Na(+)-K(+) ATPases might aggregate within the lipid rafts to fulfill their functions.

The study of single anticancer peptides interacting with HeLa cell membranes by single molecule force spectroscopy.

To determine the effects of biophysical parameters (e.g. charge, hydrophobicity, helicity) of peptides on the mechanism of anticancer activity, we applied a single molecule technique-force spectroscopy based on atomic force microscope (AFM)-to study the interaction force at the single molecule level. The activity of the peptide and analogs against HeLa cells exhibited a strong correlation with the hydrophobicity of peptides. Our results indicated that the action mode between α-helical peptides and cancer cells was largely hydrophobicity-dependent.