30 results about "Malignant phenotype" patented technology

A method for reversing expression of malignant phenotype in cancer cells is described. The method comprises applying beta 1 integrin function-blocking antibody to the cells. The method can be used to assess the progress of cancer therapy. Human breast epithelial cells were shown to be particularly responsive.

The present invention discloses a fusion protein for treating a breast cancer, wherein the fusion protein is Her2 single-chain fragment antibody-polypeptide, the Her2 single-chain fragment antibody is capable of targeting a Her2 receptor locating on a surface of a breast cancer cell, and the polypeptide is capable of carrying siRNA. The polypeptide includes a protamine polypeptide. The siRNA includes PLK1-siRNA, which is capable of restraining an expression of a knubble malignant phenotype gene. The fusion protein for treating the breast cancer is capable of carrying the PLK1-siRNA, and targeting and importing a Her2 positive breast cancer cell specifically, so as to bring the medicament into the cell. The treatment of the breast cancer is capable of generating a strong effect for restraining the breast cancer growth and transfer, may break a gene suppression effect of the existing antisense oligonucleotide and ribozyme, and becames a novel anti-Her2 gene medicament for treating the breast cancer.

Antibodies which specifically bind to components of the DNA synthesome which are altered in malignant cells are disclosed. These antibodies can be used, inter alia, to diagnose, prognoses, and treat malignancy and in assays to screen cells, tissues, and body fluids for the presence of a malignant phenotype. These antibodies can be further used to identify test compounds having the ability to suppress the malignant phenotype in a cell by assaying for the ability to inhibit or block the function of an altered component of the DNA synthesome associated with the malignant phenotype. Further, disclosed herein are methods and kit for minimally invasively detecting the presence of neoplasms and malignant conditions using easily obtainable body fluids, such as blood, plasma, lymph, pleural fluid, spinal fluid, saliva, sputum, urine, and semen, for example, to both detect the presence of cancer as well as assess the stage of the disease and the prognosis of the patient. By detecting the presence of an altered form of a component of the DNA synthesome in body fluid, one can diagnose and prognose malignancy. The disclosed method and kit therefor can be used as a diagnostic biomarker for malignancy as well as a means of monitoring the progress and effectiveness of therapeutics.

The invention discloses application of gap junction protein and coding gene thereof in preparing medicament for reversing malignant phenotype of a cancer stem cell, and investigates the functional state of gap junction communication in the tumor stem cell, expression condition of the gap junction protein and relation between the gap junction protein and special biological characteristics of tumorstem cells. Results prove that compared with differentiated tumor cells, gap junction communication obstacle exists in the tumor stem cell, no clear gap junction like structure is found among the cells, and expressions of various gap junction protein, particularly gap junction protein 43(Cx43), is down regulated; the down regulation of the expression of the Cx43 is related to promoter methylationof coding gene GJA1 thereof and expression of micro RNA; recovering of the expression of the Cx43 in the tumor stem cell can remarkably reduce the self-renew ability, tumor forming ability and invasion ability of the tumor stem cells, which is related to partial recovery of the gap junction communication function, up regulation of E-cadherin expression and inactivity of SDF-1/CXCR4 downstream signal path (AKT and ERK1/2); and the gap junction protein and coding gene thereof can be used for preparing the medicament for reversing malignant phenotype of the cancer stem cell.

The invention discloses a purpose of ATCA (Aurintricarboxylic acid, aurin tricarboxylic acid) to preparation of medicines for treating tumors. Through experiment, the inventor of the invention finds that through specifically intervening a translation initiation process, the ATCA can enable cancer cells not to strengthen malignant phenotypes through slowing down cancer gene translation elogation rate, so that the malignant phenotypes of the cancer cells can be restrained, besides, lethal effects on normal cells can be minimized, the effect of resisting cancer is achieved, and besides, the sideeffects are effectively controlled. The ATCA disclosed by the invention has important application value on tumor treatment.

The invention relates applications of vitamin C derivatives in antitumor products. According to the present invention, with the continuous and long-time administration of the low-dose vitamin C derivatives, the differentiation of cancer cells can be inhibited, and the malignant phenotype of cancer cells can be effectively inhibited, such that the evidence can be provided for the application of thevitamin C derivatives in tumor differentiation therapy.

The invention provides an application of forsythiaside A to preparation of an anti-esophageal squamous cell carcinoma medicine. The forsythiaside A is used as an active component in the anti-esophageal squamous cell carcinoma medicine, and the molecular formula of the forsythiaside A is C29H36O15. The forsythoside A mainly inhibits proliferation, clone formation and cell migration of esophageal squamous carcinoma cells, or promotes apoptosis of the esophageal squamous carcinoma cells by retarding the cycle of the esophageal squamous carcinoma cells so as to achieve the purpose of resisting the esophageal squamous carcinoma. Therefore, the forsythiaside A has an inhibiting effect on the malignant phenotype of the esophageal squamous carcinoma.

Embodiments herein provides an in vitro co-culture system comprising a population of cancer responder cells and a population of non-tumor cells wherein the cancer responder cells can convert to a malignant state and exhibit hallmark malignant phenotype when the cells are placed in a tumor supportive environment. The system is useful for prognosis evaluation of cancer recurrence, malignancy development, cancer drug screening and surveillance for resistance to cancer drug therapy.

The invention, which belongs to the field of biological medicines, particularly relates to application of an ILF3 detection reagent in preparation of a colorectal cancer diagnosis reagent and a colorectal cancer prognosis diagnosis reagent/kit. The research finds that ILF3 is overexpressed in a specimen of a primary CRC patient and is related to poor prognosis; and the gene is suggested to be possibly related to the malignant phenotype of CRC at the clinical level. With the molecular biological means, interference of ILF3 can significantly inhibit CRC proliferation, so that the ILF3 is shown to have an important function in colorectal cancer occurrence and development. In addition, the invention also discovers that the ILF3 promotes tumor growth by directly adjusting the mRNA stability ofthe SGOC gene and increasing the expression of the SGOC gene for the first time; that is, the ILF3 influences tumors by adjusting the SGOC pathway. Researches show that the SGOC inhibitor can be usedfor treating CRC patients with ILF3 overexpression and has important clinical significance.

The invention belongs to the technical field of bioinformatics, and discloses a non-differential gene associated with tumor cell malignant phenotypes and a screening method and application thereof, the non-differential gene interacts with a plurality of differential genes of cancerous tissues, is ubiquitous in the cancerous tissues and para-carcinoma tissues, has relatively high abundance expression and no differential expression, and can be used for screening tumor cell malignant phenotypes. And the characteristic of playing a heavy role in a network path is realized. And sorting the genes to be distinguished through an SVM model for distinguishing cancerous tissues and para-carcinoma tissues, and removing differential genes from the genes at the first 5% of the sorted genes to obtain the non-differential genes. With the non-differential gene as a target, the non-differential gene can be used for preparing drugs for preventing or treating tumors related to the non-differential gene. Whether the non-differential genes are knocked down for preventing tumors or knocked down after tumors are formed for controlling tumor development, the screened non-differential genes can inhibit the sizes of mice tumors.

The invention discloses an application of deubiquitinating enzyme USP28 in preparation of a medicine for preventing or treating pancreatic cancer. Research finds that USP28 expression in pancreatic cancer tumor tissue is higher than that in normal pancreatic tissue, and USP28 high expression is remarkably related to malignant phenotype and lifetime shortening of pancreatic cancer patients; overexpression of the USP28 can accelerate growth of pancreatic cancer cells, and down-regulation of the USP28 can inhibit in-vitro and in-vivo growth of the pancreatic cancer cells; USP28 promotes the growth of pancreatic cancer cells by accelerating the cell cycle process and inhibiting cell apoptosis. In the aspect of mechanism, USP28 is subjected to ubiquitination and stabilizes a transcription factor FOXM1, which is a key medium for Wnt/beta-catenin signal transduction, USP28-mediated FOXM1 stabilizes and significantly promotes beta-catenin nucleation so as to further cause activation of a Wnt/beta-catenin pathway, and recovery of FOXM1 expression can alleviate the antitumor effect caused by down regulation of USP28. The deubiquitinating enzyme USP28 promotes the development of the pancreatic cancer by enhancing FOXM1 mediated Wnt/beta-catenin signal channel activation, and a powerful means is provided for potential targeted treatment and prevention of pancreatic cancer patients in the future.

Tryptophan degradation is a key metabolic pathway controlling immune reactions and evidence suggests that during cancer progression generation of tryptophan metabolites may be fundamental for immune escape promoting the malignant phenotype of cancer cells in an autocrine fashion. The invention relates to methods of measuring mass tag labelled tryptophan and metabolites thereof and methods using the labelled molecules for monitoring in a subject the effectiveness of a treatment and of disease recurrence after treatment, for stratifying patients and for diagnosing suppression of an immune response in a subject.

Disclosed is a novel intracellular response nanoparticle loaded with target gene siRNA. The novel intracellular response nanoparticle comprises a high-molecular polymer PDSA which wraps the target gene siRNA and is decomposed under the glutathione concentration in cytoplasm, and the nanoparticle at least simultaneously wraps two kinds of target gene siRNA, namely MGLL-siRNA and CB2-siRNA. The nanoparticle capable of releasing siRNA through decomposition under the cytoplasmic glutathione concentration is utilized, the defect of siRNA transmission in the prior art is overcome, intracellular glutathione can be quickly responded, and the siRNA transmission efficiency is improved. The nanoparticles simultaneously wrap MGLL-siRNA and CB2-siRNA, so that malignant phenotype genes of malignant tumors can be silenced, repolarization of tumor-related macrophages to anti-cancer phenotypes can be promoted, MGLL expression is knocked down to directly act on the malignant tumors for inhibition, and CB2 is knocked down to promote repolarization of the tumor-related macrophages to M1 type to synergistically resist tumors.

The invention discloses a human miR-183 gene cluster biological knock-down element, a construction method and an application thereof. Sequence is as shown in the SEQ ID NO:1. Abnormal expression of miR-183 gene cluster exists in many tumor cells, and the family participates in regulation of cell proliferation, apoptosis and cell migration related genes. Through design of the gene cluster knock-down element, expression of a gene cluster in bladder cancer cell can be effectively regulated. The knock-down element of the invention is convenient for scientific research and is also helpful for controlling tumor malignant phenotype and biological behavior.

The invention discloses a human miR-210 biological knock-down element, a construction method and an application thereof. Sequence of the biological knock-down element is as shown in the SEQ ID NO:1. Abnormal expression of miR-210 exists in many tumor cells, and the family participates in regulation of cell proliferation, apoptosis and cell migration related genes. Through design of the knock-down element, expression of miR-210 in bladder cancer cell can be effectively regulated. The knock-down element of the invention is convenient for scientific research and is also helpful for controlling tumor malignant phenotype and biological behavior.

The invention discloses tRF related to pancreatic cancer. The nucleotide sequence of the tRF related to pancreatic cancer is shown as SEQ ID No. 1. The present invention finds a tRNA-derived fragmenttRF-21-VBY having a function of highly expressing a malignant phenotypic function that significantly inhibits pancreatic cancer cells, which has the ability to inhibit cell proliferation, migration and invasion, promotes apoptosis, inhibits subcutaneous transplantation tumor growth and pancreatic cancer in-situ tumor growth, and can indicate the prognosis of pancreatic cancer patients. Therefore,the tRF-21-VBY or the activator thereof can be used for preparing a medicine for treating pancreatic cancer or screening a medicine suitable for treating pancreatic cancer; the reagent for detecting tRF-21-VBY can be used for preparing a pancreatic cancer prognosis prediction kit.

The invention discloses application of CEBP alpha as a detection reagent of an RANBP2 target site in preparation of glycosylation related medicine for treating liver cancer. Researches show that high expression of RANBP2 in liver cancer cells is positively correlated with liver cancer malignant phenotypes, and RANBP2 down-regulates OGA expression and increases O-glycosylation modification, so that proliferation and invasion abilities of the liver cancer cells are improved. As a key transcription factor CEBP alpha for forward regulation of OGA, RANBP2 can induce SUMOylation of the CEBP alpha, and experiments prove that the K196 site of the CEBP alpha is the SUMO key target site of the RANBP2, and the SUMOylation of the site can promote CEBP alpha protein degradation. OGA-mediated O-glycosylation pathways can be slowed down by protecting the K196 site of the CEBP alpha from being influenced by SUMOylation modification or improving the expression of the CEBP alpha.