Multiple myeloma (MM) is a malignant plasma cell disease that currently cannot be cured. Several new drugs have continuously been introduced in the recent years. New drugs targeting B-cell maturation antigen (BCMA) have greatly improved the efficacy and prognosis of MM compared with traditional treatments. This article reports the case of an IgD type relapsed and refractory MM patient with poor efficacy of BCMA×CD3 bispecific antibody. The patient achieved deep remission after receiving BCMA-targeted CAR-T cell therapy after initial seven lines of treatment. Literature review was also conducted to improve the clinical physicians’ understanding of BCMA target therapy for relapsed and refractory MM patients.

Objective: To determine the changed expression levels, biological roles and underlying mechanism of LncSox4 in non-small cell lung cancer (NSCLC), providing novel biomarkers for NSCLC diagnosis and therapy. Methods: QRT-PCR was used to detect the expression of LncSox4 in the tumor tissues of NSCLC patients. Colony formation, cell growth curve, Transwell migration and invasion assays were used to determine the effects of LncSox4 knockdown on A549 cell function, respectively. Flow cytometry was used to determine the effects of LncSox4 on the progression of A549 cell cycle. QRT-PCR and western blot were used to explore the expressions of genes and proteins in epithelial-mesenchymal transition (EMT). Results: The expression of LncSox4 was upregulated significantly in carcinoma tissues of NSCLC compared to the para-carcinoma tissues (t=7.109，P＜0.01). The growth rate of A549 cells slowed down in LncSox4 knockdown group and the number of formed cell colonies was less than that in control group(P＜0.01). LncSox4 knockdown reduced the migration and invasion abilities of A549 cells (P＜0.01) and induced cell cycle arrest at G1 phase(P＜0.01). LncSox4 knockdown downregulated the protein expressions of Cyclin D1, c-Myc, N-cadherin, and Vimentin, while upregulated the expression of E-cadherin in A549 cells. LncSox4 knockdown also decreased the expressions of EMT-related transcription factors including snail, slug and twist. Conclusion The high expression of LncSox4 in NSCLC may promote malignant progression of NSCLC by enhancing cell proliferation, migration and invasion, suggesting that it should be a promising target for diagnosis and therapy of NSCLC.

Objective: To investigate the expression change, biological role and action mechanism of long non-coding RNA (lncRNA) LINC00978 in non-small cell lung cancer (NSCLC). Methods: The expression levels of LINC00978 in tumor tissues and serum samples of NSCLC patients were detected by the qRT-PCR. The effects of knockdown and overexpression of LINC00978 on the biological function of A549 cells were determined by the CCK-8, colony formation, Transwell migration and invasion assays. The action mechanisms of LINC00978 in NSCLC were investigated by the flow cytometry, qRT-PCR and western blot, respectively. Results: The expression levels of LINC00978 in the tissues ( t =2.465, P ＜0.05) and serum samples ( t =8.781, P ＜0.01) of NSCLC patients increased. The knockdown of LINC00978 inhibited the proliferation, migration and invasion of A549 cells ( P ＜0.01) and induced cell cycle arrest at G1 phase and apoptosis of A549 cells ( P ＜0.01). The knockdown of LINC00978 downregulated the expression of Cyclin D1 and Bcl-2 , and upregulated the expression of Bax ( P ＜0.05). In addition, the knockdown of LINC00978 inhibited the expression of N-cadherin, Vimentin, Snail, Slug and Twist, and promoted the expression of E-cadherin ( P ＜0.05). The overexpression of LINC00978 had the opposite effect. Conclusion LINC00978 is highly expressed in NSCLC and can promote the occurrence and progression of NSCLC, which may serve as a potential target for the diagnosis and therapy of NSCLC.