Kirkpatrickburch1376
Currently, the patient remains recurrence-free 17 months after the initial diagnosis. PT2399 cell line This report presents the first case demonstrating the coexistence of L-FLAC and AIS in the same pulmonary nodule, harboring different genetic mutations. Based on the literature review, this is the second reported case of L-FLAC bearing DICER1 mutations.
Breast cancer is one of the most common and malignant tumors in the world. Nowadays more attention has been garnered in pristimerin anti-cancer effects. Here, we illustrate the function and regulatory mechanism of pristimerin in breast cancer therapy.
Breast cancer cell lines MCF-7, MDA-MB-231, and 4T1 were used. Cell Counting Kit-8 (CCK-8) assay was performed to evaluate proliferation viability of breast cancer cells under pristimerin treatment. Wound healing assay was used to examine the migration ability, cell cycle, and cell apoptosis detection were tested by flow cytometry. Bioinformatic analysis was used to find the underlying molecular and gene connected with pristimerin and breast cancer survival. Finally, we used transfection and real-time polymerase chain reaction analysis to confirm the mechanism.
We observed that pristimerin inhibited breast cancer cell viability, migration, and cell cycle, meanwhile induced cell apoptosis. In addition, under pristimerin treatment, miR-542-5p was up-regulated while DUB3 was down-regulated. Furthermore, bioinformatics analysis showed higher expression of DUB3 in breast cancer compared with normal tissue, also with poor prognosis. Overexpression miR-542-5p in breast cancer cells leads to a decrease in DUB3 level. The effect was obviously post pristimerin treatment and miR-542-5p overexpression.
Pristimerin inhibited breast cancer progression through DUB3 expression via a canonical miRNA-mediated mechanism.
Pristimerin inhibited breast cancer progression through DUB3 expression via a canonical miRNA-mediated mechanism.Multitargeted antiangiogenic drugs have demonstrated significant antitumor activity against a variety of solid tumors. Anlotinib, a novel oral multitargeted antiangiogenic tyrosine kinase inhibitor, was approved as a third-line treatment for advanced NSCLC in China. However, predictive biomarkers are currently insufficient and are urgently required. Herein, we report three pre-treated cases of advanced NSCLC with TP53 mutations, wherein these patients showed partial response to anlotinib. Moreover, the three patients have achieved a progression-free survival of 8, 6.5, and 5 months, respectively. The main toxicities were hypertension, hand-foot syndrome and fatigue. In conclusion, TP53 mutations may represent a biomarker for predicting salutary effects of anlotinib.
As the first-line drug for treatment of
-positive metastatic gastric cancer (GC), Herceptin exhibits significant therapeutic efficacy. However, acquired resistance of Herceptin limits the therapeutic benefit of gastric cancer patients, in which the molecular mechanisms remain to be further determined.
Quantitative real-time polymerase chain reaction was performed to detect the mRNA levels of
and
in GC cells. Protein levels were determined using Western blot and IHC staining. MTT and soft agar colony formation assays were used to measure cell proliferation. Xenograft model was established to verify the functional role of
in Herceptin resistance in vivo. Sphere formation assay was conducted to determine cell stemness.
We observed
was up-regulated in Herceptin resistance gastric cancer cells NCI-N87-HR and MKN45-HR. The forced expression of
promoted, whereas the silencing of
impaired Herceptin resistance of
-positive gastric cancer cells both in vitro and in vivo. Moreover,
significantly enhanced the sphere formation capacity and
expression,
was also a positive factor of Herceptin resistance in
-positive gastric cancer cells. In addition, high level of
was positively associated with Herceptin resistance and poor survival rate of gastric cancer patients.
We have demonstrated that
promoted Herceptin resistance of gastric cancer via up-regulation of
, our study suggested that
could be a potential diagnostic and therapeutic candidate for
-positive gastric cancer.
We have demonstrated that ARPP-19 promoted Herceptin resistance of gastric cancer via up-regulation of CD44, our study suggested that ARPP-19 could be a potential diagnostic and therapeutic candidate for HER2-positive gastric cancer.MicroRNAs (miRNAs) are endogenous, non-coding, single-stranded, tiny RNAs with 21-23 nucleotides that regulate several biological functions through binding to target mRNAs and modulating gene expression at post-transcriptional levels. Recent studies have described crucial roles for miRNAs in pathophysiology of numerous human cancers. They can act as an oncogene and promote cancer or as a tumor suppressor and alleviate the disease. Recently discovered microRNA-154 (miR-154) has been proposed to be involved in multiple physiological and pathological processes including cancer. With this aspect, aberrant expression of miR-154 has been demonstrated in variety of human malignancies, suggesting an important role for miR-154 in tumorigenesis. To be specific, it is considered as a tumor suppressor miRNA and exerts its beneficial effects by targeting several genes. This review systematically summarizes the recent advances done on the role of miR-154 in different cancers and discusses its potential prognostic, diagnostic and therapeutic values.
To investigate the clinicopathologic and prognostic significance of the zinc-finger protein 711 (ZNF711) in breast cancer (BCa).
The relevance of ZNF711 in BCa was analyzed using bioinformatics. The expression of ZNF711 was detected by immunohistochemistry in paraffin blocks of BCa. To evaluate its clinical significance, the correlation between the expression of ZNF711 and BCa clinical indicators, including estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor-2 (HER-2), was analyzed. Finally, the Kaplan-Meier method was applied to explore the prognostic value of ZNF711.
ZNF711 expression was decreased in BCa and was negatively correlated with ER expression (
< 0.05) and positively correlated with HER-2 expression (
< 0.01), but there was no significant correlation between ZNF711 and PR expression. ZNF711 expression was not correlated with age, tumor diameter, or lymph node metastasis; however, ZNF711 expression was correlated with staging in BCa. Survival analysis results showed that the ZNF711-positive group patients had a poorer prognosis compared with the ZNF711-negative group.
