Traditional Chinese Medicine Syndromes are Associated with Driver Gene Mutations and Clinical Characteristics in Patients with Lung Adenocarcinoma.

This study aimed to investigate the associations between traditional Chinese medicine (TCM) syndromes and driver gene mutations as well as the clinical characteristics of patients with lung adenocarcinoma. We performed a cross-sectional study in patients with lung adenocarcinoma between June 2020 and October 2021. The patient characteristics, such as age, sex, smoking history, clinical stage, metastasis, driver gene mutations, and the type of traditional Chinese medicine syndrome/element, were collected. The associations between each TCM syndrome and sex, smoking history, clinical stage, metastasis, and driver gene mutations were analyzed. The present study included 127 patients. The most frequent TCM syndromes were Qi and Yin deficiency (39, 30.7%) and lung-spleen Qi deficiency (32, 25.2%). Eighty-one (63.8%) patients had mutations in driver genes, especially in the EGFR gene (64, 79.0%). There was a statistically significant association between a driver gene mutation and TCM syndrome (P < 0.05). Genetic mutations presented more frequently in patients with Qi and Yin deficiency (37.0%), lung-spleen Qi deficiency (30.0%), or the cold element (59.3%). Male patients were more likely to have Qi stagnation and blood stasis, whereas female patients were more likely to have lung-spleen Qi deficiency or Qi and Yin deficiency. The patients with lung-spleen Qi deficiency were usually younger than those with Qi and Yin deficiency or Qi stagnation and blood stasis (P < 0.05). Compared with the patients with other TCM syndromes, the patients with Yin and Yang deficiency were more likely to have bone metastasis. TCM syndromes were associated with driver gene mutations, sex, age, and bone metastasis in patients with lung adenocarcinoma.

Frontier progress of the combination of modern medicine and traditional Chinese medicine in the treatment of hepatocellular carcinoma.

Hepatocellular carcinoma (HCC, accounting for 90% of primary liver cancer) was the sixth most common cancer in the world and the third leading cause of cancer death in 2020. The number of new HCC patients in China accounted for nearly half of that in the world. HCC was of occult and complex onset, with poor prognosis. Clinically, at least 15% of patients with HCC had strong side effects of interventional therapy (IT) and have poor sensitivity to chemotherapy and targeted therapy. Traditional Chinese medicine (TCM), as a multi-target adjuvant therapy, had been shown to play an active anti-tumor role in many previous studies. This review systematically summarized the role of TCM combined with clinically commonly used drugs for the treatment of HCC (including mitomycin C, cyclophosphamide, doxorubicin, 5-fluorouracil, sorafenib, etc.) in the past basic research, and summarized the efficacy of TCM combined with surgery, IT and conventional therapy (CT) in clinical research. It was found that TCM, as an adjuvant treatment, played many roles in the treatment of HCC, including enhancing the tumor inhibition, reducing toxic and side effects, improving chemosensitivity and prolonging survival time of patients. This review summarized the advantages of integrated traditional Chinese and modern medicine in the treatment of HCC and provides a theoretical basis for clinical research.

The Shuganhuazheng Formula in Triple-Negative Breast Cancer: A Study Based on Network Pharmacology and In Vivo Experiments.

Breast cancer is the most common cancer in women. Among breast cancer subtypes, triple-negative breast cancer (TNBC) has the highest degree of malignancy and the worst prognosis. The Shuganhuazheng formula (SGHZF) is a traditional Chinese herbal formula for the treatment of TNBC, but the mechanism of SGHZF in the treatment of TNBC remains unclear. In this study, the therapeutic effect and mechanism of SGHZF against TNBC were preliminarily determined based on in vivo experimental verification and network pharmacology. In terms of therapeutic effects, the antitumour effect was verified by measuring and calculating tumour volume, and the expression of proto-oncogene c-Myc was verified by PCR. In terms of the mechanism, potential therapeutic targets were identified by overlapping the SGHZF-related and TNBC-related targets. After comprehensively analysing the results of the protein-protein interaction (PPI), gene ontology (GO) function, and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analyses, Akt and HIF-1α were selected for verification by using immunohistochemical and Western blot analyses. The results of the study indicated that SGHZF can inhibit breast tumour growth in mice and that the mechanism may be related to the inhibition of Akt and HIF-1α expression.

LncRNA CASC15 promotes colon cancer cell proliferation and metastasis by regulating the miR­4310/LGR5/Wnt/ß­catenin signaling pathway.

Previous studies have indicated that overexpression of long noncoding RNA cancer susceptibility 15 (CASC15) may promote tumor development and progression in gastric cancer and hepatocellular carcinoma. However, the function of CASC15 in colon cancer remains unknown. In the present study, the expression of CASC15 was upregulated in colon cancer tissues and its expression was correlated with clinical Tumor­Node­Metastasis stage and tumor metastasis. In addition, knockdown of CASC15 significantly inhibited the proliferation, migration and invasion of colon cancer cells in vitro and in vivo. Following mechanistic experiments, CASC15 was observed to act as a sponge to suppress microRNA (miR)­4310 that targeted LGR5. Through the inhibition of miR­4310, CASC15 promoted leucine­rich repeat­containing G­protein coupled receptor 5 (LGR5) expression and consequently activated the Wnt/ß­catenin signaling pathway. The results revealed that the inhibition of the Wnt/ß­catenin signaling pathway in CASC15­overexpressing colon cancer cells suppressed cellular proliferation, migration and invasion. Collectively, these results demonstrated that CASC15 promoted colon cancer growth and metastasis through the activation of the Wnt/ß­catenin signaling pathway in a miR­4310/LGR5 dependent manner. Thus, the present study suggested that CASC15 may be a therapeutic target for colon cancer treatment.

Long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 regulates the expression of Gli2 by miR-202 to strengthen gastric cancer progression.

BACKGROUND: Gastric cancer (GC) is one of the most common malignancies and ranks the second leading cause of cancer death worldwide. Some studies had reported the tumor-promoting effects of long non-coding RNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) as a competing endogenous RNA (ceRNA) by sponging to microRNAs. However, the molecular mechanism of ceRNA regulatory pathway involving MALAT1 in GC remains unclear. METHODS: MALAT1 and miR -202 expression was detected by quantitative real time PCR (qRT-PCR) in 60 gastric cancer tissues and adjacent normal tissues, CCK8 cell proliferation assays, cell cycle analysis and cell apoptosis assays were performed to detect the GC cell proliferation and apoptosis. The mRNA and protein levels of Gli2 were analyzed by quantitative real-time PCR and Western blotting assays. Furthermore, using online software, luciferase reporter assays, RNA immunoprecipitation (RIP) and RNA pulldown assays demonstrated miR-202 was a target of MALAT1. RESULTS: We found that MALAT1 was upregulated in GC tissues and higher MALAT1 expression was correlated with larger tumor size, lymph node metastasis, and TNM stage. Moreover, we revealed that MALAT1 was a direct target of miR-202 and knockdown of MALAT1 significantly decreased the expression of Gli2 through negatively regulating miR-202. In addition, knockdown of Malat1 inhibited GC cells proliferation, S-phase cell number, and induced cell apoptosis via negatively regulating miR-202 in vitro. CONCLUSIONS: Our results elucidated MALAT1/miR-202/Gli2 regulatory pathway, which maybe contribute to a novel therapeutic strategy for GC patients.

LMO1 is a novel oncogene in lung cancer, and its overexpression is a new predictive marker for anti-EGFR therapy.

Non-small cell lung cancer (NSCLC) is the leading cause of cancer mortality in the world. We report that one oncogene amplified on chromosome 3q26, LMO1, a master transcriptional regulator of stemness, operates to drive strong growth phenotype in NSCLC. We first validate gene expression changes of LMO genes by real-time quantitative RT-PCR real-time quantitative reverse transcriptase-polymerase chain reaction analysis and immunohistochemistry, and we identified gene overexpression of LMO1 compared with non-cancerous tissues (p < 0.01). Next, we discovered that LMO1 promoted cancer cell proliferation in our in vitro/vivo cell proliferation assay, and our cell signaling experiments showed that LMO1 expression correlated with elevated AKT phosphorylation in NSCLC, while the AKT phosphorylation was required for LMO1's oncogenic effects. In addition, we compared complete response rate, stable disease rate, disease progression rate, and the disease control rate of patient with different LMO1 gene expression which pointed to the usefulness of LMO1 overexpression, as a new predictive marker for responsiveness to cetuximab. All in all, LMO1 is a commonly activated tumor promoter that activates AKT signaling in NSCLC and a new predictive marker for targeted therapy.

LMO1 is a novel oncogene in colorectal cancer and its overexpression is a new predictive marker for anti-EGFR therapy.

Colorectal cancer (CRC) is the third leading cause of cancer mortality in the world. We report that one oncogene amplified on chromosome 3q26, LMO1, a master transcriptional regulator of stemness, operates to drive strong growth phenotype in CRC. The gene expression changes of LMO1 in human CRC tissues compared with noncancerous tissues were detected using real-time quantitative reverse transcriptase-polymerase chain reaction (QRT-PCR) analysis and immunohistochemistry, which identified the gene overexpression of LMO1 in CRC. Moreover, we discovered that LMO1 promoted cancer cell proliferation in vitro/in vivo and LMO1 expression correlated with elevated AKT phosphorylation in CRC while the AKT phosphorylation was required for oncogenic effects of LMO1. Next, our data point to the usefulness of LMO1 overexpression, as a new predictive marker for responsiveness to cetuximab. All in all, LMO1 is a commonly activated tumor promoter that activates AKT signaling in CRC and a new predictive marker for targeted therapy.

[Electroacupuncture at Zusanli (ST 36) for treatment of nausea and vomiting caused by the chemotherapy of the malignant tumor: a multicentral randomized controlled trial].

OBJECTIVE: To compare the clinical effects between electroacupuncture at Zusanli (ST 36) combined with intravenous drip of Granisetron and intravenous drip of Granisetron only for treatment of nausea and vomiting caused by the chemotherapy of the malignant tumor. METHODS: The methods of multicentral, randomized controlled trial were used, the observation group (127 cases) was treated with electroacupuncture at Zusanli (ST 36) combined with intravenous drip of Granisetron, and the control group (119 cases) was treated with intravenous drip of Granisetron only. RESULTS: The total effective rate of 90.5% in observation group was superior to that of 84.0% in control group (P < 0.01); the nausea and vomiting scores of two groups were obviously decreased after treatment (both P < 0.001), and the decreased degree of the observation group was superior to that of control group (P < 0.001). CONCLUSION: Electroacupuncture at Zusanli (ST 36) can significantly alleviate the symptoms such as nausea and vomiting caused by the chemotherapy of the patients.