ABSTRACT
OBJECTIVES: To investigate the effects of myelin- and lymphocyte-associated protein (MAL) gene knockout on the morphological structure of lung tissue and the expression of E-cadherin (E-cad) and alpha-smooth muscle actin (α-SMA) in an asthmatic mouse model. METHODS: Twenty-four specific pathogen-free (SPF) C57BL/6J mice were divided into four groups: the wild-type normal (WT/SAL), wild-type asthmatic (WT/OVA), gene knockout normal (MAL-/-/SAL), and gene knockout asthmatic (MAL-/-/OVA) groups. The establishment of the asthma mouse models was confirmed by evaluating behavioral symptoms and histopathological H&E and Masson staining. Western blotting and RT-qPCR were used to measure E-cad and α-SMA expression levels in lung tissues. RESULTS: H&E staining of mouse lung tissues from WT/OVA, MAL-/-/SAL, and MAL-/-/OVA groups revealed a thickened bronchial wall, irregular lumen edge, locally fallen mucosal epithelium, and inflammatory cell infiltration compared with those of the WT/SAL group. In the WT and MAL-/- groups, the proportion of Masson-stained tissues in the OVA group was greater than that in the SAL group (p < 0.05). Compared with those in the WT/SAL group, the expression levels of α-SMA mRNA and protein were increased, while those of E-cad were decreased in the WT/OVA group (p < 0.01). Similarly, compared with those in the MAL-/-/SAL group, the expression levels of E-cad mRNA and protein were increased, while those of α-SMA were decreased in the MAL-/-/OVA group (p < 0.01). All these differences were statistically significant (p < 0.01). CONCLUSIONS: The MAL gene contributes to EMT inhibition and the stability of the airway barrier under normal physiological conditions by regulating E-cad and α-SMA expression.
ABSTRACT
Saccharomyces cerevisiae MCD4 is a 2-deoxyglucose (2-DOG)-resistant mutant derived from the wild-type strain, AK46, wherein the 2-DOG resistance improves the maltose fermentative ability. In the MAL gene cluster, mutations were detected in MAL11 and MAL31, which encode maltose permeases, and in MAL13 and MAL33, which encode transcriptional activators. In maltose medium, the expression of MAL11 and MAL31 in MCD4 was 2.1 and 4.2 times significantly higher than that in AK46, respectively. Besides, the expression of MAL13 and MAL33 also tended to be higher than that of AK46. Although no mutations were found in MAL12 and MAL32 (which encode α-glucosidases), their expression was significantly higher (4.9 and 4.4 times, respectively) than that in AK46. Since the expression of major catabolite repression-related genes did not show significant differences between MCD4 and AK46, these results showed that the higher maltose fermentative ability of MCD4 is due to the activation of MAL genes encoding two maltose permeases and two α-glucosidases.
ABSTRACT
MAL gene expresses in the mediate and late stage of T-lymphocytes.Many studies have shown that the expression of MAL gene has down regulation or loss in many kinds of tumors including esophageal carcinoma,gastric cancer,colon cancer,head and neck squamous cell carcinoma,and so on.MAL gene is related with the process of generation and development of the tumors.The application of MAL gene for clinical diagnosis,prognostic and instructing therapy needs further studies.
ABSTRACT
MAL gene expresses in the mediate and late stage of T-lymphocyte,correlated with carcinoma.Hereditary factors and epigenetic mechanisms play important roles in the pathogenesis of colorectal carcinoma.One of the main epigenetic modifications to be identified is methylation of DNA.the hypermethylation and abnormal expressions of MAL gene play a key role in the development,invasion,metastasis and prognosis of colorectai carcinoma.Therefore MAL gene may be another promising early diagnostic marker,which provide new evidence for early stage prediction,classification,prognosis,chemoprevention of colorectal carcinoma.
ABSTRACT
Objective To investigate the mechanisms of Mal gene down regulated in human esophageal cancer. Methods We amplified the 5′regulatory region of Mal gene in normal placenta tissue and human esophageal cancer cell lines EC9706、EC8712、EC109 by optimization the PCR methods, cloned and sequenced the PCR products and compare the sequence. Results Human esophageal cancer cell lines EC9706、EC8712、EC109 all have the 654 th of 5′regulatory region of Mal gene T to C changes, corresponding codon changed from TCC to CCC, and the amino acid which it codes changed from serine to proline; EC9706 also has the 657 th of 5′regulatory region of Mal gene T to C changes, corresponding codon changed from TGC to CGC, the amino acid which it codes changed from cysteine to arginine; EC8712 has the 139 th of 5′regulatory region of Mal gene A to G changed, corresponding codon changed from GGA to GGG, the amino acid which it codes remains glycine. Conclusion Our results suggested there are may point mutation in 5′ region of Mal gene in human esophageal cancer.