PEMANFAATAN WADAH BERBAGI PENGETAHUAN DAN KUALITAS MEREK TERHADAP PERILAKU LOYALITAS KONSUMEN

In this study, a brand of herbal medicine called Red Kank (cancer suppression) which was originally described strongly as a cancer reducer but has now evolved into something more than cancer-fighting products, such as health and beauty products. This strategic step has not been able to answer whether it leads to the company's success, but it opens the possibility to assess the quality of brand relationships, use of knowledge sharing platforms and their impact on consumer loyalty behavior Red Kank. Primary data were collected using purposive sampling technique from customers in Jakarta, Bekasi, Surabaya and Balikpapan. The results were then run with lisrel 8.7 and analyzed by Structural Equation Modeling (SEM). Statistical results show that the quality of the brand relationship is closely related to the image of the quality of the product itself. Therefore, the company's strategy to diversify, begins with increasing understanding of product brands to become company brands.

Review Article: Vitamin C Progress Apoptosis in Breast Cancer

The cancer of breast is virulence in female and is curable in ~70–80% of patients. The vitamin type C is an essential vitamin and consider as an anti-oxidant, so this vitamin could recover the supply for oxygen, stopping the destroy of DNA and other impact necessary in cancer processing. The vitamin C indicate as an active anticancer as the concentricity were monitor in this cancer therapy. The concentricity of this vitamin has a main function in cancer-rising or cancer suppression. These studies have shown a relationship between the vitamin and increase death-rate of breast cancer, so it’s important to detect the anticancer prospective of vitamin C to detect the different among its effect in healthy and damage cells, especially these studies conducted that this difference could depend on the vitamin c concentration. These studies indicate that large doses of vitamin c could decrease the effect of some cancer therapy such as radiation and chemotherapy.

Upregulation of DNA repair genes and cell extrusion underpin the remarkable radiation resistance of Trichoplax adhaerens

Trichoplax adhaerens is the simplest multicellular animal with tissue differentiation and somatic cell turnover. Like all other multicellular organisms, it should be vulnerable to cancer, yet there have been no reports of cancer in T. adhaerens or any other placozoan. We investigated the cancer resistance of T. adhaerens, discovering that they are able to tolerate high levels of radiation damage (218.6 Gy). To investigate how T. adhaerens survive levels of radiation that are lethal to other animals, we examined gene expression after the X-ray exposure, finding overexpression of genes involved in DNA repair and apoptosis including the MDM2 gene. We also discovered that T. adhaerens extrudes clusters of inviable cells after X-ray exposure. T. adhaerens is a valuable model organism for studying the molecular, genetic, and tissue-level mechanisms underlying cancer suppression.

Region-Specific Biomarkers and Their Mechanisms in the Treatment of Lung Adenocarcinoma: A Study of Panax quinquefolius from Wendeng, China

Panax quinquefolius, a popular medicinal herb, has been cultivated in China for many years. In this work, the region-specific profiles of metabolites in P. quinquefolius from Wendeng was investigated using liquid-chromatography–quadrupole–time-of-flight-(LC–Q–TOF)-based metabolomics analysis. The three most abundant biomarkers, identified as ginsenoside Rb3, notoginsenoside R1, and ginsenoside Rc, were the representative chemical components employed in the network pharmacology analysis. In addition, molecular docking and western blotting analyses revealed that the three compounds were effective binding ligands with Hsp90α, resulting in the inactivation of SRC and PI3K kinase, which eventually led to the inactivation of the Akt and ERK pathways and lung cancer suppression. The outcomes obtained herein demonstrated the intriguing chemical characteristics and potential functional activities of P. quinquefolius from Wendeng.

The ethanol extract of Garcinia subelliptica Merr. induces autophagy

Background Garcinia subelliptica Merr. is a multipurpose coastal tree, the potential medicinal effects of which have been studied, including cancer suppression. Here, we present evidence that the ethanol extract of G. subelliptica Merr. (eGSM) induces autophagy in human lung adenocarcinoma cells. Methods Two different human lung adenocarcinoma cell lines, A549 and SNU2292, were treated with varying amounts of eGSM. Cytotoxicity elicited by eGSM was assessed by MTT assay and PARP degradation. Autophagy in A549 and SNU2292 was determined by western blotting for AMPK, mTOR, ULK1, and LC3. Genetic deletion of AMPKα in HEK293 cells was carried out by CRISPR. Results eGSM elicited cytotoxicity, but not apoptosis, in A549 and SNU2292 cells. eGSM increased LC3-II production in both A549 and, more extensively, SNU2292, suggesting that eGSM induces autophagy. In A549, eGSM activated AMPK, an essential autophagy activator, but not suppressed mTOR, an autophagy blocker, suggesting that eGSM induces autophagy by primarily activating the AMPK pathway in A549. By contrast, eGSM suppressed mTOR activity without activating AMPK in SNU2292, suggesting that eGSM induces autophagy by mainly suppressing mTOR in SNU2292. In HEK293 cells lacking AMPKα expression, eGSM increased LC3-II production, confirming that the autophagy induced by eGSM can occur without the AMPK pathway. Conclusion Our findings suggest that eGSM induces autophagy by activating AMPK or suppressing mTOR pathways, depending on cell types.

Breast cancer suppression by curcumin-naringenin-magnetic-nano-particles: In vitro and in vivo studies

BACKGROUND: The limitations of surgery, radiotherapy, and chemotherapy in cancer treatment and the increase in the application of nanomaterials in the field of biomedicine have promoted the use of nanomaterials in combination with radiotherapy for cancer treatment. OBJECTIVE: To improve the efficiency of cancer treatment, curcumin-naringenin loaded dextran-coated magnetic nanoparticles (CUR-NAR-D-MNPs) were used as chemotherapy and in combination with radiotherapy to verify their effectiveness in treating tumors. METHODS: CUR-NAR-D-MNPs were prepared and studied by several characterization methods. Median inhibitory concentration (IC50) and cellular toxicity were evaluated by 3-(4,5-dimethylthiazolyl-2)-2,5-diphenyltetrazolium bromide (MTT) assay. The cell death and radiosensitization were studied by acridine orange/ethidium bromide dual staining of MCF-7 human breast cancer cells. RESULTS: CUR-NAR-D-MNPs induce apoptosis and inhibited cell proliferation through reactive oxygen species (ROS) generation. CUR-NAR-D-MNPs used alone had a certain therapeutic effect on tumors. CUR-NAR-D-MNPs plus radiotherapy significantly reduced the tumor volume and led to cell cycle arrest and induction of apoptosis through modulation of P53high, P21high, TNF-αlow, CD44low, and ROShigh signaling CONCLUSIONS: CUR-NAR-D-MNPs are effective in the treatment of tumors when combined with radiotherapy, and show radiosensitization effects against cancer proliferation in vitro and in vivo.

Potential Role of Exercise Induced Extracellular Vesicles in Prostate Cancer Suppression

Physical exercise is increasingly recognized as a valuable treatment strategy in managing prostate cancer, not only enhancing supportive care but potentially influencing disease outcomes. However, there are limited studies investigating mechanisms of the tumor-suppressive effect of exercise. Recently, extracellular vesicles (EVs) have been recognized as a therapeutic target for cancer as tumor-derived EVs have the potential to promote metastatic capacity by transferring oncogenic proteins, integrins, and microRNAs to other cells and EVs are also involved in developing drug resistance. Skeletal muscle has been identified as an endocrine organ, releasing EVs into the circulation, and levels of EV-containing factors have been shown to increase in response to exercise. Moreover, preclinical studies have demonstrated the tumor-suppressive effect of protein and microRNA contents in skeletal muscle-derived EVs in various cancers, including prostate cancer. Here we review current knowledge of the tumor-derived EVs in prostate cancer progression and metastasis, the role of exercise in skeletal muscle-derived EVs circulating levels and the alteration of their contents, and the potential tumor-suppressive effect of skeletal muscle-derived EV contents in prostate cancer. In addition, we review the proposed mechanism of exercise in the uptake of skeletal muscle-derived EVs in prostate cancer.

Suppression of MIR31HG Affects the Functional Properties of Thyroid Cancer Cells Depending on miR-761/MAPK1 Axis

Background: Long non-coding RNAs (lncRNAs) possess pivotal roles in human cancers, including thyroid cancer. In this study, we sought to elucidate the precise action of MIR31HG in the functional behaviors of thyroid cancer cells.Methods: MIR31HG, microRNA (miR)-761 and mitogen-activated protein kinase 1 (MAPK1) were quantified by quantitative real-time PCR (qRT-PCR) or immunoblotting analysis. Cell viability, proliferation, apoptosis, invasion, and migration abilities were evaluated by MTS, 5-Ethynyl-2’-Deoxyuridine (EdU), flow cytometry, transwell and wound-healing assays, respectively. Dual-luciferase reporter assays were performed to validate the relationship between miR-761 and MIR31HG or MAPK1. Mouse xenografts were formed to assess the effect of MIR31HG on tumor growth.Results: MIR31HG expression was at high levels in thyroid cancer. Suppression of MIR31HG impeded cell proliferation, invasion, and migration, as well as promoted cell apoptosis in vitro, and diminished the growth of xenograft tumors in vivo. Mechanistically, MIR31HG targeted and regulated miR-761. Moreover, the effects of MIR31HG suppression was partly dependent on increased abundance of miR-761. MAPK1 was established as a direct and functional target of miR-761. Furthermore, MIR31HG involved the modulation of MAPK1 expression through competitively binding to miR-761 by the shared binding sequence.Conclusion: Our findings demonstrate the workings of an undescribed regulatory network, in which MIR31HG targets miR-761 to regulate MAPK1 expression, leading to the alteration of the functional behaviors of thyroid cancer cells.