Knockdown of KIF26B inhibits breast cancer cell proliferation, migration, and invasion

Gu, Shudong; Liang, Haibin; Qi, Donghui; L, Mao; Mao, Guoxin; Li, Qian; Zhang, Shu

doi:10.2147/ott.s163346

Cited by 28 publications

(28 citation statements)

References 27 publications

(31 reference statements)

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“…For instance, previous reports revealed that up-regulation of KIF14 could promote cancer progression and metastasis, and could predict poor prognosis in gastric cancer and colorectal cancer [23,24]. Gu et al suggested that silencing of KIF26B suppressed breast cancer cell growth and invasion [25]. KIFC1 is also reported to be participated in the progression of NSCLC through regulation of cell proliferation and cell cycle [7].…”

Section: Discussionmentioning

confidence: 99%

“…It's well known that uncontrolled proliferation is a prominent feature of malignant tumors. Gu et al showed that depletion of KIF26B triggers cell cycle could arrest through regulating CyclinD1 to modulate cell proliferation in mammary cancer [25]. Liu et al showed that knockdown of KIFC1 could reduce cell proliferation and trigger G2/M phase arrest in A549 and SPC-A1 cells [7].…”

Section: Discussionmentioning

confidence: 99%

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Kinesin superfamily protein 21B acts as an oncogene in non-small cell lung cancer

et al. 2020

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Background: Kinesin superfamily proteins (KIFs) serve as microtubule-dependent molecular motors, and are involved in the progression of many malignant tumors. In this study, we aimed to investigate the expression pattern and precise role of kinesin family member 21B (KIF21B) in non-small cell lung cancer (NSCLC). Methods: KIF21B expression in 72 cases of NSCLC tissues was measured by immunohistochemical staining (IHC). We used shRNA-KIF21B interference to silence KIF21B in NSCLC H1299 and A549 cells and normal lung epithelial bronchus BEAS-2B cells. The biological roles of KIF21B in the growth and metastasis abilities of NSCLC cells were measured by Cell Counting Kit-8 (CCK8), colony formation and Hoechst 33342/PI, wound-healing, and Transwell assays, respectively. Expression of apoptosis-related proteins was determined using western blot. The effect of KIF21B on tumor growth in vivo was examined using nude mice model. Results: KIF21B was up-regulated in NSCLC tissues, and correlated with pathological lymph node and pTNM stage, its high expression was predicted a poor prognosis of patients with NSCLC. Silencing of KIF21B mediated by lentivirusdelivered shRNA significantly inhibited the proliferation ability of H1299 and A549 cells. KIF21B knockdown increased apoptosis in H1299 and A549 cells, down-regulated the expression of Bcl-2 and up-regulated the expression of Bax and active Caspase 3. Moreover, KIF21B knockdown decreased the level of phosphorylated form of Akt (p-Akt) and Cyclin D1 expression in H1299 and A549 cells. In addition, silencing of KIF21B impeded the migration and invasion of H1299 and A549 cells. Further, silencing of KIF 21B dramatically inhibited xenograft growth in BALB/c nude mice. However, silencing of KIF21B did not affect the proliferation, migration and invasion of BEAS-2B cells. Conclusions: These results reveal that KIF21B is up-regulated in NSCLC and acts as an oncogene in the growth and metastasis of NSCLC, which may function as a potential therapeutic target and a prognostic biomarker for NSCLC.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Kinesin superfamily protein 21B acts as an oncogene in non-small cell lung cancer

et al. 2020

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“…For instance, previous reports reveal that up-regulation of KIF14 is positively associated with cancer progression and poor prognosis of cancer of the prostate gland and epithelial ovarian cancer patients [19,20]. Gu S et al suggests that silencing of KIF26B suppresses breast cancer cell growth and invasion [21]. KIFC1 is also reported to participate in the progression of NSCLC through regulation of cell proliferation and cell cycle [7].…”

Section: Discussionmentioning

confidence: 99%

“…regulates cell invasion in breast cancer through driving epithelial-mesenchymal transition (EMT) [21].…”

Section: Discussionmentioning

confidence: 99%

Kinesin superfamily protein 21B acts as an oncogene in non-small cell lung cancer

Sun

Pan

Shao

et al. 2020

Preprint

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Background Kinesin superfamily proteins (KIFs) serve as microtubule-dependent molecular motors, and are involved in the progression of many malignant tumors. In this study, we aimed to investigate the expression pattern and precise role of KIF21B in non-small cell lung cancer (NSCLC). Methods KIF21B expression in 72 cases of NSCLC tissues was measured by immunohistochemical staining (IHC). We used shRNA-KIF21B interference to silenced KIF21B in NSCLC cells. The biological roles of KIF21Bin the growth and metastasis abilities of NSCLC cells were measured by CCK8, colony formation and Hoechst/PI, wound-healing, and Transwell assays. The effect of KIF21B on tumor growth in vivo was examined using nude mice model. Results KIF21B was up-regulated in NSCLC tissues and correlated with pathological lymph node and pTNM stage, its high expression was predicted a poor prognosis of patients with NSCLC. Silencing of KIF21B mediated by lentivirus-delivered shRNA significantly inhibited the proliferation ability of H1299 cells. Moreover, KIF21B knockdown increased H1299 cell apoptosis through modulating the Bcl-2/Bax and active Caspase 3 expression. KIF21B knockdown decreased p-Akt expression and Cyclin D1 expression in H1299 cells. In addition, silencing of KIF21B impeded H1299 cell migration and invasion. Further, silencing of KIF 21B dramatically inhibited xenograft growth in BALB/c nude mice. Conclusions These results reveal that KIF21B is up-regulated in NSCLC and acts as an oncogene in the NSCLC progression.

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“… 58 The prognosis of endocrine-related breast cancer and HER2-positive breast cancer has improved due to effective antitumor drugs. 59 , 60 However, the prognosis and clinical outcomes of TNBC, which does not express estrogen receptors (ER), progesterone receptors (PR) or HER2, are far from satisfying. 61 , 62 Although TNBC only accounts for a small portion (10%–20%) of all breast cancer cases, it has a high mortality risk and is more aggressive than other breast cancer sub-types.…”

Section: Discussionmentioning

confidence: 99%

MicroRNA-645 targets urokinase plasminogen activator and decreases the invasive growth of MDA-MB-231 triple-negative breast cancer cells

Du¹,

Lei²,

Han³

et al. 2018

OTT

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BackgroundUrokinase plasminogen activator (uPA) promotes the in vivo invasive growth of HCC cells by cleaving and activating matrix metalloproteinases (MMPs) to induce the destruction of the extracellular matrix of triple-negative breast cancer (TNBC) cells. The identification of microRNAs that target uPA and decrease uPA expression would be useful for attenuating the in vivo invasive growth of TNBC cells.Materials and methodsMicroRNA-645 (miR-645) was identified using an online tool (miRDB) as potentially targeting uPA; miR-645 inhibition of uPA was confirmed by western blot experiments. The effects of miR-645 on the in vivo invasive growth of TNBC cells were examined using an intrahepatic tumor model in nude mice, and the miR-645 mechanism of action was explored with MMP cleaving experiments.ResultsThrough virtual screening, we discovered that miR-645 potentially targeted the uPA 3′ untranslated region. This targeting was confirmed by western blot experiments and miR-645 lentiviral particle (LV-645) transduction that inhibited uPA expression in MDA-MB-231 TNBC cells. The LV-645 inhibition of uPA led to the decreased invasive growth of TNBC cells in nude mice. The mechanism data indicated that the uPA inhibition resulted in a decreased cleaving of the pro-MMP-9 protein.ConclusionTargeting uPA with miR-645 decreased the in vivo invasive growth of TNBC cells. These results suggest that miR-645 may represent a promising treatment strategy for TNBC.

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Knockdown of KIF26B inhibits breast cancer cell proliferation, migration, and invasion

Cited by 28 publications

References 27 publications

Kinesin superfamily protein 21B acts as an oncogene in non-small cell lung cancer

Kinesin superfamily protein 21B acts as an oncogene in non-small cell lung cancer

Kinesin superfamily protein 21B acts as an oncogene in non-small cell lung cancer

MicroRNA-645 targets urokinase plasminogen activator and decreases the invasive growth of MDA-MB-231 triple-negative breast cancer cells

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