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Berberine is an isoquinoline alkaloid present in several plant species, including Coptis sp. and Berberis sp. In traditional medicine, extracts of berberine are used in the treatment of diarrhea of different origins. Recent studies have shown that berberine and its derivatives have significant biological effects on gastrointestinal (GI) and other functions and may become therapeutics for the treatment of diarrhea, gastroenteritis, diabetes, hyperlipidemia, cardiovascular diseases and inflammatory conditions. This paper summarizes the current knowledge on the actions of berberine in the GI tract. Binding and target sites, activated intracellular pathways, as well as the absorption and metabolism of berberine are discussed. Effects that may be useful in future clinical treatment, like antidiarrheal, anti-inflammatory and antitumor effects are critically reviewed and potential clinical applications are presented in detail.

Qu-Yu-Jie-Du decoction (QYJD) is a commercially available traditional Chinese medicine (TCM). It is an aqueous extract of a Chinese herbal formula primarily consisting of eight TCM herbs: Taraxacum campylodes G.E. Haglund, Coix lacryma-jobi L., Smilax glabra Roxb., Sanguisorba officinalis L, Styphnolobium japonicum (L.) Schott, Prunus persica (L.) Batsch, Sophora flavescens Aiton, and Eupolyphaga sinensis Walker. Matrine and oxymatrine are two of the major phytochemical constituents of QYJD. Inflammation and oxidative stress are strongly associated with colon carcinogenesis. Colorectal cancer (CRC) is the third most common type of cancer. Therefore, cancer chemopreventive agents targeting CRC are urgently needed. This study was conducted to investigate the potential anticancer effects and the underlying mechanisms of QYJD and its active constituents, matrine and oxymatrine, in human colon cancer HT29 cells and in a dextran sulfate sodium (DSS)-induced colitis mouse model. QYJD and matrine effectively inhibited the proliferation and anchorage-independent growth of HT29 cells in a dose-dependent manner. QYJD and matrine also induced an Nrf2-mediated anti-oxidant response element-luciferase activity and upregulated the Nrf2-mediated anti-oxidative stress genes HO-1 and NQO1 at both the mRNA and protein levels. In the DSS-induced colitis mouse model, QYJD reduced the disease activity index (DAI) and alleviated colonic shortening. Elevated Nrf2 and HO-1 mRNA levels were also observed in QYJD-treated mice. These findings showed that QYJD could elicit anti-inflammatory and anti-oxidative stress response in vitro in a cell line and in vivo in a DSS-induced colitis mouse model. These responses may contribute to the overall anticolon cancer effect of QYJD.

Cinobufacini is a well-known Chinese medicine extracted from Venenum Bufonis, also called Chan Su. It has been used clinically for various cancers, including colon cancer. However, the function of Cinobufacini on colon cancer invasion and metastasis, and its underlying molecular mechanism, is still not clear. In this study, we investigated the function and mechanism of Cinobufacini on colon cancer invasion and metastasis both in vitro and in vivo studies. Human colon cancer cells were cultured. CCK assay was used to detect the effect of Cinobufacini on colon cancer cells proliferation. The invasion and migration abilities were observed by transwell assays, and the expression of invasion and migration related genes MMP2, MMP9, and epithelial-to-mesenchymal transition (EMT) relate genes were observed by Western blot assays. An orthotopic xenograft model in nude mice was established using colon cancer HCT116 cells, and the function of Cinobufacini on colon cancer invasion and metastasis were observed in vivo. We found Cinobufacini significantly inhibited colon cancer cell proliferation in a dose/time-dependent manner; the invasion and migration abilities of colon cancer were decreased after treated with Cinobufacini. The metastasis and EMT related genes MMP9, MMP2, N-cadherin and Snail were obviously down-regulated, while the expression of E-cadherin was up-regulated after treatment with Cinobufacini. The Wnt/$\beta$-catenin signaling pathway related genes were observed using WB,and results show that the expression of $\beta$-catenin, wnt3a, c-myc, cyclin D1, and MMP7 were all down-regulated after being treated with cinobufacini, while the expression of APC was up-regulated. In vivo studies of the volume and weight of orthotopic xenograft tumors showed significantly shrinkage in the Cinobufacini group compared to the control group. The enterocoelia and liver metastasis tumors were significantly decreased, and the expression of MMP9, MMP2, and $\beta$-catenin were also down-regulated, while E-cadherin was up-regulated in vivo after the treatment with Cinobufacini. Our data proves that Cinobufacini can inhibit colon cancer invasion and metastasis both in vitro and in vivo; the mechanism is related by suppressing the Wnt/$\beta$-catenin signaling pathway and then inhibiting the EMT of CRC.

Bauhinia championii (Benth.) is one of the commonly used herbs in Taiwan. The stem of this plant has been used to treat epigastria pain and rheumatoid arthritis. However, the antitumor activities of this herb have never been reported. This study aims to investigate the mechanism of anticancer activity of the extracts from B. championii (BC). BC was fractionated with a series of organic solvents, including n-hexane (H), ethyl acetate (EA), 1-butanol (B), and water (W). We first investigated the effects of BC-H, BC-EA, BC-B and BC-W partitioned fraction on cell viability. In HCT 116 colon cancer cell lines, BC-EA showed the highest inhibition of cell viability and changed the morphology of cells. With dose- and time-dependent manners, BC-EA inhibited the proliferation of HCT 116 cells by inducing apoptosis and G₀/G₁ phase arrest of cell cycle. To determine the underlying mechanisms, down-regulated CDK2, Cyclin D, and Cyclin E and up-regulated p16, p21, and p53 may account for the cell cycle arrest, while the apoptotic effect of BC-EA may attribute to increased intracellular Ca${}^{2+}$, loss of mitochondria membrane potential ($\mathrm{\Delta }{\mathrm{\Psi }}_m$), increase of Bax, Bak, puma, and AIF, and decrease of Bcl-2. Furthermore, the inactivation of Ras signaling pathway by BC-EA also contributed to its apoptotic effect on HCT 116. Our study demonstrates that BC-EA not only inhibits cell growth but also induces apoptosis through inhibiting Ras signal pathway and increasing p53 expression levels. We suggest that BC-EA may be a new dietary supplement and a useful tool to search for therapeutic candidates against colon cancer.

Over-expression of calpains in tumor tissues can be associated with cancer progression. Thus, inhibition of calpain activity using specific inhibitors has become a novel approach to control tumor growth. In this study, the anticancer potential of cryptotanshinone in combination with calpain inhibitor had been investigated in colon cancer cells and tumor xenograft. Cryptotanshinone elicited an initial endoplasmic reticular (ER) stress response, whereas prolonged stress would result in the promotion of apoptosis. It was then discovered that cryptotanshinone could cause rapid and sustained increase in cytosolic calcium in colon cancer cells accompanied by early GRP78 overexpression, which could be attenuated by pre-treatment of the calcium chelator BAPTA-AM. Cryptotanshinone also facilitated an early increase in calpain activity, which could be blocked by BAPTA-AM or the calpain inhibitor PD150606. A dynamic interaction between GRP78 and calpain during the action of cryptotanshinone was unveiled. This together with the altered NF-$\kappa$B signaling could be abolished by calpain inhibitor. GRP78 knockdown increased the sensitivity of cancer cells to cryptotanshinone-evoked apoptosis and reduction of cancer cell colony formation. Such sensitization of drug action had been confirmed to be p53-dependent by using p53-mutated (HT-29) and p53-deficient (HCT116 p53^−∕−) cells. The synergistic antitumor effect of cryptotanshinone and calpain inhibitor was further exhibited in vivo. Taken together, findings in this study exemplify a new chemotherapeutic regimen comprising cryptotanshinone and calpain inhibitor by regulation of calpain and calcium homeostasis. This has provided us with new insights in the search of a potential target-specific neoadjuvant therapy against colon cancer.

Invasion and metastasis are the major causes leading to the high mortality of colon cancer. Ginsenoside Rg3 (Rg3), as a bioactive ginseng compound, is suggested to possess antimetastasis effects in colon cancer. However, the underlying molecular mechanisms remain unclear. In this study, we reported that Rg3 could effectively inhibit colon cancer cell invasion and metastasis through in vivo and in vitro studies. In addition, Rg3 suppressed the epithelial–mesenchymal transition (EMT) of HCT15 cells and SW48 cells evidenced by detecting EMT related markers E-cadherin, vimentin, and snail expression. Furthermore, inhibition of Notch signaling by LY411,575 or specific Hes1 siRNA obviously repressed colon cancer cell migration and metastasis, and induced increase in E-cadherin and decrease in vimentin and snail. Meanwhile, the expression of NICD and Hes1 was obviously decreased in the presence of Rg3. However, Rg3 failed to suppress EMT in Hes1 overexpressed colon cancer cells. In particular, Rg3 significantly reversed IL-6-induced EMT promotion and blocked IL-6- induced NICD and Hes1 upregulations. Overall, these findings suggested that Rg3 could inhibit colon cancer migration and metastasis via suppressing Notch-Hes1-EMT signaling.

The molecular mechanism underlying the anticancer effects of Anemarrhena asphodeloides (A. asphodeloides) on colon cancer is unknown. This is the first study evaluating the anticancer effect of A. asphodeloides extract (AA-Ex) in serum-starved colorectal cancer cells. Changes in cell proliferation and morphology in serum-starved MC38 and HCT116 colorectal cancer cells were investigated using MTS assay. Cell cycle and apoptosis were investigated using flow cytometry, and cell cycle regulator expression was determined using qRT-PCR. Apoptosis regulator protein levels and mitogen-activated protein kinase (MAPK) phosphorylation were assessed using western blotting. AA-Ex sensitively suppressed proliferation of serum-starved colorectal cancer cells, with MC38 and HCT116 cells showing greater changes in proliferation after treatment with AA-Ex under serum starvation than HaCaT and RAW 264.7 cells. AA-Ex inhibited cell cycle progression in serum-starved MC38 and HCT116 cells and increased the expression of cell cycle inhibitors (p53, p21, and p27). Furthermore, AA-Ex induced apoptosis in serum-starved MC38 and HCT116 cells. Consistently, AA-Ex suppressed the expression of the anti-apoptotic molecule Bcl-2 and upregulated pro-apoptotic molecules (cytochrome c, cleaved caspase-9, cleaved caspase-3, and cleaved-PARP) in serum-starved cells. AA-Ex treatment under serum starvation decreased AKT and ERK1/2 phosphorylation in the cell survival signaling pathway but increased p38 and JNK phosphorylation. Furthermore, AA-Ex treatment with serum starvation increased the levels of the transcription factors of the p38 and JNK pathway. Serum starvation sensitizes colorectal cancer cells to the anticancer effect of A. asphodeloidesvia p38/JNK-induced cell cycle arrest and apoptosis. Hence, AA-Ex possesses therapeutic potential for colon cancer treatment.

Colon cancer, a common type of malignant tumor, seriously endangers human health. However, due to the relatively slow progress in diagnosis and treatment, the clinical therapeutic technology of colon cancer has not been substantially improved in the past three decades. The present study was designed to investigate the effects and involved mechanisms of schisandrin B in cell growth and metastasis of colon cancer. C57BL/6 mice received AOM and dextran sulfate sodium. Mice in treatment groups were gavaged with 3.75–30 mg/kg/day of schisandrin B. Transwell chamber migration, enzyme-linked immunosorbent assay (ELISA), Western blot analysis, immunoprecipitation (IP) and immunofluorescence were conducted, and HCT116 cell line was employed in this study. Data showed that schisandrin B inhibited tumor number and tumor size in the AOD+DSS-induced colon cancer mouse model. Schisandrin B also inhibited cell proliferation and metastasis of colon cancer cells. We observed that schisandrin B induced SMURF2 protein expression and affected SIRT1 in vitro and in vivo. SMURF2 interacted with SIRT1 protein, and there was a negative correlation between SIRT1 and SMURF2 expressions in human colorectal cancer. The regulation of SMURF2 was involved in the anticancer effects of schisandrin B in both in vitro and in vivo models. In conclusion, the present study revealed that schisandrin B suppressed SIRT1 protein expression, and SIRT1 is negatively correlated with the induction of SMURF2, which inhibited cell growth and metastasis of colon cancer. Schisandrin B could be a leading compound, which will contribute to finding novel potential agents and therapeutic targets for colon cancer.

Hypoxic microenvironment and dysregulated endoplasmic reticulum stress/unfolded protein response (UPR) system are considered important factors that promote cancer progression. Although osthole extracted from Cnidium monnieri(Fructus Cnidii) has been confirmed to exhibit an anticancer activity in various cancers, the effects of osthole in hypoxic colon cancer cells have not been explored. Therefore, the aim of this study was to examine whether osthole has an inhibitory effect on hypoxic colon cancer HCT116 cells and further investigate the underlying molecular mechanisms. Treatment with osthole significantly attenuated the cell viability, proliferation, and migration in hypoxic HCT116 cells. Osthole also activated UPR signaling such as phospho-eukaryotic initiation factor 2 alpha (EIF2$\alpha )$/ATF4/CHOP/DR5 cascade accompanied by upregulation of pro-apoptotic proteins. Moreover, the tubule-like formation of human umbilical vein endothelial cells, the secretion of vascular endothelial growth factor A, and the expression and activity of hypoxia-inducible factor-1$\alpha$ (HIF-1$\alpha )$ in hypoxic HCT116 cells were markedly suppressed by osthole. However, suppressing EIF2$\alpha$ phosphorylation with salubrinal or ISRIB markedly reversed the effects of osthole on the expressions of pro-apoptotic proteins and HIF-1$\alpha$. Co-treatment of hypoxic HCT116 cells with osthole greatly increased the sensitivity to cisplatin and the expressions of phospho-EIF2$\alpha$ and cleaved caspase 3. Collectively, the inhibitory effect of osthole in hypoxic HCT116 cells may be associated with EIF2$\alpha$ phosphorylation-mediated apoptosis and translational repression of HIF-1$\alpha$. Taken together, osthole may be a potential agent in the treatment of colon cancer.

Baicalin was reported to facilitate the apoptosis of colon cells and inhibit tumor growth in vivo. This study aimed to explore the specific mechanism and function of baicalin on colon cells. Relative mRNA levels were tested via qPCR. Cell proliferation, viability, and cell cycle phases were evaluated using MTT, colony formation, and flow cytometry assays, respectively. The interaction between miR-139-3p and cyclin-dependent kinase 16 (CDK16) was measured via a dual-luciferase reporter assay. Immunohistochemistry was used to count the positivity cells in tumor tissues collected from treated xenografted tumor mice. The results showed that baicalin increased miR-139-3p expression while also decreasing CDK16 levels, blocking the cell cycle, and inhibiting cell proliferation in colon cancer cells. miR-139-3p silencing or CDK16 overexpression abolished the inhibitory effects of baicalin on colon cancer proliferation. miR-139-3p directly targeted and interacted with CDK16 at the cellular level. The protective functions of miR-139-3p knockdown on tumor cells were abrogated by silencing CDK16. The combination of baicalin treatment and CDK16 knockdown further inhibited tumor growth of xenografted tumor mice compared with the groups injected with only sh-CDK16 or baicalin in vivo. In conclusion, baicalin inhibited colon cancer growth by modulating the miR-139-3p/CDK16 axis.

Genetic Links to Breast Cancer Uncovered.

Malaria’s Complete Genome Sequenced.

Australian Study Finds Good News for HRT.

Gene Mapping for Cancer, Heart Diseases.

Japan Sees Improvements to Research Methodology Vital.

Tall Men Susceptible to Colon Cancer.

New Study Offers Hope For Parkinson’s Disease.

Singapore Researcher Develops Hair Loss Remedy.

Twin Goats Successfully Cloned in Taiwan.

Japanese Researchers Made Progress in Stem Cells Research.

New Genetic-based Predictive Models for Lung Cancer Relapse.

Alcohol Doubles the Chance of Colon Cancer.

Taiwanese Researchers Discover Rare Skin Disease Genes.

GM Tobacco Plant Model for Rabies Antibody Production.

Indian Scientists Find Cure for Black Fever.

Stem Cell Research at Reliance Ready for Animal Trials.

Colon Cancer More Likely to Kill Obese Women.

Auckland University Researchers Recreate Original Ancestor of HIV Virus.

The Ultimate Solution for Breast Cancer Patients?

New Zealand Scientists Discover New Family of Cancer Genes.

Kenya Research Laboratory Develops Anti-virus Sweet Potatoes.

AUSTRALIA — UWA Researchers Link New Gene to Osteoporosis.

AUSTRALIA — Australian Surgeons Save Unborn Baby's Leg.

CHINA — China Honors IRRI for Contributions to Food Security and Science.

CHINA — Chinese Red Yeast Rice Extract Reduces Repeat Heart Attacks/Mortality Rates.

CHINA — Cholesterol Absorbing Mechanism Unveiled.

CHINA — Academia Sinica and BASF to Develop Rice Strains.

HONG KONG — Hong Kong Scientists Make New Bird Flu Breakthrough.

INDIA — Mirrus Opens India R&D center.

INDIA — United States Launches Rs 580 million Health Initiative in India.

INDIA — IBSD to Analyze Herb with Cancer Curing Property.

INDIA — Rare Heart Surgery at Delhi Hospital.

JAPAN — First Optical Pacemaker: Laser Controls Beating Of Heart Muscle Cells in Cell Culture.

SINGAPORE — Singapore-led Team Starts S$3.5 Million Liver Cancer Clinical Trial.

SINGAPORE — Wealth of Genomic Hotspots Discovered in Embryonic Stem Cells.

SINGAPORE — Scientists Identify Genetic Regulator of Colon Cancer and Develop a Novel Therapeutic Strategy for Colon Cancer Treatment.

SINGAPORE — First Confirmed Common Genetic Risk Factors for Breast Cancer Uncovered by Genome Institute of Singapore and Partners in international Breast Cancer Association Collaboration.

AUSTRALIA — Prototype Test for Predicting Clinical Outcome for Melanoma Patients

AUSTRALIA — New Model Predicts Long-term Survival of Critically Ill Patients

AUSTRALIA — World's First Computerized System to Predict Premature Births

CHINA — Biomagnetics (BMGP) Enters Chinese Biotech Market

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INDONESIA — Indonesia's Pharmaceutical Companies Get Boost in Competitive Advantage from Launch of Newport Horizon Premium and IDRAC Solutions

INDIA — India's Government Nods to Set up 10 Testing Units for Ayurvedic Drugs

INDIA — DuPont India Opens First Research Facility in Hyderabad

INDIA — CSIR and Godavari Sugar to Set up India's First Sugarcane Biorefinery

INDIA — FRLHT Develops Herbal Drug for Diabetes Mellitus

INDIA — Chhattisgarh Government to Set Up Herbal Medicinal Park to Promote Industry

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INDIA — India Develops Hybrid Mustard Seed, Better Yield Expected

INDIA — Hindustan Latex to Develop MediPark

NEW ZEALAND — NZ Bird Flu “Could Mutate into More Serious Form”

NEW ZEALAND — HRC Invests Over $1.07 million to Help Build International Health Research Partnerships

SINGAPORE — Singapore Researchers Find Key Gatekeeper Gene that Plays Key Role in Colon Cancer

SINGAPORE — Singapore Research Produces Plastic Micro Needles that can be Mass-Produced More Easily and Cheaply for Painless Injections and Extraction of Bodily Fluids

SINGAPORE — Singapore Researchers Develop New Stem Cell Therapy for Heart Disease

SINGAPORE — Singapore's First Commercial Developer of Molecular Diagnostic Assays Commences Operation

SINGAPORE — Singapore to Host Medical Equipment Manufacturing Show

VIETNAM — Local Scientists Create Sperm from Stem Cells

VIETNAM — Vietnam to Reinforce Crackdown on Fake Medicine

KOREA – Why are Korean eggs salmonella-free?

NETHERLANDS – Breaking bad: cancer cell drug addiction solved.

SINGAPORE – Singapore researchers create new ‘letters’ to enhance DNA functions.

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TAIWAN – New insights on breast cancer therapy.

USA – Genetically boosting the nutritional value of corn could benefit millions.

A panel of nitro substituted 5,15-diaryl-porphyrins, featuring nitro groups either on the phenyl rings or on one of the two free meso-positions, was synthesized. In the former category, compounds 5-(3-nitrophenyl)-15-phenylporphyrin, 5,15-di(3-nitrophenyl)porphyrin and 5-(4-nitrophenyl)-15-phenylporphyrin were obtained following standard procedures by reacting dipyrromethane and aromatic aldehydes. In the latter category, porphyrins 10-nitro-5,15-diphenylporphyrin, 10-nitro-5-(3-methoxyphenyl)-15-phenylporphyrin and 10-nitro-5,15-di(3-methoxyphenyl)porphyrin were generated by nitration of 5,15-diarylporphyrins with trifluoroacetic acid/sodium nitrite under particularly mild conditions. The new molecules bearing one or two nitro-groups were tested as photosensitizers during in vitro experiments on a human colon adenocarcinoma cell line (HCT116), and their effects were compared with those induced by temoporfin, porfimer sodium and by some previously published electron-rich diarylporphyrins. The results, expressed as IC₅₀ values obtained by the MTT test following 24 h incubation with the photosensitizers and 2 h irradiation with a 500 W tungsten-halogen lamp, indicate that the presence of an electron withdrawing substituent, on a meso-position, decreases the photodynamic activity of the compound. Conversely, 5-(3-nitrophenyl)-15-phenylporphyrin, a non symmetrically substituted diarylporphyrin bearing both one electron-deficient and one lipophilic moiety, resulted in high phototoxic activity.

Viability of cancer cell is an important indicator of physiological state and function of cells, which can be effected by the change of pH in the medium solution, due to the increase of carbon oxide and lactic acid caused by respiration. Although many methods have been developed to detect the viability of cells, mostly based on cytochemical staining and polymerase chain reaction (PCR) technology are time consuming. In this paper, an electronic device was made by thermal reduced graphene oxide (RGO) for detection of cancer cell viability in real-time. This electronic device could be used to monitor the metabolic activity and viability of cancer cells based on the change in pH value. As the pH decreases, colon cancer cells loose viability and the current decreases. This RGO device is simple, sensitive and label-free and could serve as a platform for detection of cells and drug testing.

Early-stage disease and cancer diagnosis are of particular importance for effective patient identification as well as their treatment. Breath analysis is a promising method for this purpose which can help to detect disease biomarkers. Benzaldehyde and Indole gas molecules as members of volatile organic compounds (VOCs) are composed of a proportion of the exhaled breath and changes in the level of them from breath can be considered for colorectal cancer biomarkers. Due to these incentives, we scrutinized the sensing behavior of Molybdenum disulfide (MoS${}_2)$ toward Benzaldehyde and Indole gas. We inspected the adsorption of the molecules on the pristine and Pd-, Pt-decorated MoS₂ by employing density functional nonequilibrium Green’s function (DFT-NEGF). It was disclosed that the molecules were weakly adsorbed upon the pristine MoS₂. Howbeit, after the decoration of the surface, the adsorption energy and charge transfer of the molecules were improved greatly. On the other hand, the band gap was decreased after metal decoration. For example, adsorption energy of −2.37eV and band gap of 1.32eV were achieved by interaction of Indole with Pd-decorated MoS₂ and it can be desorbed under UV light and at temperature of 698K with recovery time of 12.8s. Ergo, our analysis would help us better understand the adsorption mechanism of Pd- and Pt-decorated MoS₂-based gas sensors. It may open a new route in early disease detection and colorectal cancer monitoring.

Spatially resolved characterization of the transcriptome and proteome promises to provide further clarity on cancer pathogenesis and etiology, which may inform future clinical practice through classifier development for clinical outcomes. However, batch effects may potentially obscure the ability of machine learning methods to derive complex associations within spatial omics data. Profiling thirty-five stage three colon cancer patients using the GeoMX Digital Spatial Profiler, we found that mixed-effects machine learning (MEML) methods^† may provide utility for overcoming significant batch effects to communicate key and complex disease associations from spatial information. These results point to further exploration and application of MEML methods within the spatial omics algorithm development life cycle for clinical deployment.